Alzheimer's disease, the most common form of dementia, has beaten back potential treatments for decades. Past research suggested it was a complicated, multifactorial disease in which a patchwork of biological and lifestyle factors combined to increase or decrease risk.

But a new study published in January in the journal Nature suggests the risk of developing the disease is determined largely by one key gene, called apolipoprotein E (APOE). Lifestyle and environmental factors can dial the risk up or down modestly in people with susceptible gene variants, but those who have protective versions of the APOE gene are extremely unlikely to develop Alzheimer's. And a staggering 99% of the population carries at least one disease-fueling version of the gene.

The findings raise the possibility that gene therapy targeting APOE could dramatically reduce the risk of Alzheimer's for a large swath of people who are at risk of developing the disease, thus paving the way for one of the first widely used gene therapies, experts told Live Science.

There are more than 900,000 people in the United States who have the highest-risk form of APOE, said Nolan Townsend, CEO of gene therapy company Lexeo Therapeutics, which is developing a therapy targeting the gene.

"There's been no gene therapy to date that's tried to address a population of that size," Townsend told Live Science.

An elusive treatment

For decades, there were no good treatments for Alzheimer's disease. No medicines actually slowed the disease's progression until the advent of anti-amyloid antibodies like donanemab, which clear the characteristic amyloid plaques that are a hallmark of the disease. But these drugs, touted as the first disease-modifying treatments for the condition, have severe side effects, including swelling and microbleeds in the brain. The patients most at risk from Alzheimer's are also most vulnerable to these side effects.

At first glance, the APOE gene wouldn't seem very relevant to Alzheimer's disease. The main role of the protein it codes for is to ferry fat molecules through the bloodstream. However, the APOE protein also closely interacts with what is considered the best-known molecular culprit in Alzheimer's: the protein amyloid-beta, which aggregates into plaques that destroy connections between neurons and trigger inflammation.

There are three versions of the APOE gene ‪—‬ APOE2, APOE3 and APOE4 ‪—‬ and each codes for a slightly different version of the protein. For decades, researchers thought that APOE2 was a protective variant, while APOE4 increased the risk of the disease. APOE3 was thought to neither increase nor decrease the risk.

But in past work, APOE2 was underrepresented; the allele is present in less than 1% of the population. In the new Nature study, which looked at data from 450,000 people, the gene trio's true contributions were revealed. APOE3 is not neutral, the study found; rather, it increases Alzheimer's risk, albeit to a much lesser extent than APOE4 does. Carrying two copies of APOE2, meanwhile, made people almost immune to developing Alzheimer's.

It's not clear why, but other research in lab dishes shows that the highest-risk variant of APOE impairs the processing of fats in support cells called glia and that this can trigger dysfunction and neuro-inflammation. APOE4 also seems to increase cell death and impairs how well cells react to oxidative stress, a state of imbalance between antioxidants and reactive chemicals called free radicals. It also impairs synaptic plasticity, or the ability to adaptively strengthen or weaken connections between brain cells.

The study authors concluded that APOE3 and APOE4 together are responsible for between 72% and 93% of Alzheimer's disease cases.

"Without strong underlying risks from APOE ε3 [APOE3] and ε4 [APOE4], almost all AD [Alzheimer's disease] and half of all dementia would not occur," the study authors noted in the paper.

That finding is buttressed by other work hinting that APOE2 is strongly protective. A 2020 study found that someone with two copies of APOE2 has a 200 times lower risk of developing Alzheimer's than someone with two copies of APOE4. Carrying just one copy of the APOE2 gene lowers the risk 80-fold.

The research raises the possibility that people with higher-risk variants might stave off the disease if they had one or two copies of the APOE2 version of the gene.

Gene therapy for the masses

That's where gene therapy comes in.

Gene therapies have transformed the lives of people with rare genetic disorders, such as the muscle-wasting disease spinal muscular atrophy (SMA) and a progressive form of blindness called retinal dystrophy. In these cases, the therapy involves delivering a copy of a healthy gene into a tissue that lacks it.

But these treatments target tiny populations; SMA, for example, affects about 1 in 15,000 live births in the United States. Some gene therapy approaches are customized for just a single patient.

By contrast, the study estimates that about 28% of the population carries at least one copy of the highest-risk versions of the APOE gene that could potentially benefit from this drug.

Mayur Parmar, a pharmacologist at NOVA Southeastern University in Florida, has conducted studies of APOE2 gene therapies in mice.

"As we have learned in recent years, APOE4 plays an important role in terms of amyloid beta, tau, neuroinflammation, and oxidative stress. It can be a potential target, Parmar told Live Science. APOE2 therapies could work by suppressing these effects, he added.

Now, these ideas are being put to the test. New York City-based Lexeo Therapeutics plans three safety and dosing clinical trials to increase protective APOE gene variants and reduce harmful APOE gene variants in people with the highest-risk gene APOE4/APOE4 gene combination who have early Alzheimer's disease.

The first phase of their research is a combined safety and dosing study that incorporates the protective APOE2 gene variant into the brains of people with early Alzheimer's. A second study, which has not yet reached the human testing phase, will instead add a version of APOE2 that has the ultrarare Christchurch mutation, a rare variant found in the brains of people who show no Alzheimer's symptoms despite having severe amyloid plaque buildup.

Researchers think the Christchurch variant is like a souped-up version of APOE2 that will offer even more neuroprotection. Finally, the team is planning a trial combining the addition of APOE2 with using tiny snippets of RNA to suppress APOE4 gene expression, which they hope will enhance the therapeutic effect.

The company's initial safety testing showed that the therapy was well-tolerated and reduced tau levels in most of the 15 participants recruited. Only topline results from the study have been published, although Townsend said that long-term cognitive data from the trial will eventually be released.

The ability of APOE gene therapies to target multiple disease pathways could offer patients significant benefits, but it will be tough to prove. Pharmaceutical companies like Lexeo must choose a clinical outcome, like better memory preservation or less amyloid buildup, to demonstrate to regulators that their therapies work. The most obvious signs that a therapy works are detected through behavioral and cognitive testing, but trials pegged to those outcomes are massive in scope and cost, said Townsend. That's because it can take years for the effects of a promising treatment to manifest and because such testing is quite expensive on its own.

The pharma companies that developed anti-amyloid antibodies bypassed this need because the U.S. Food and Drug Administration (FDA) agreed to view reduced amyloid load in the brain as a proxy for cognitive improvement. However, this approach has been controversial because of the uncertain link between these molecular changes and cognitive benefits, and Townsend said the regulatory environment for genetic therapies is less permissive.

"There's uncertainty in the regulatory frameworks and landscape to get to an accelerated approval of a genetic-focused approach in this area," Townsend said.

Crossing the barrier

Another challenge is getting the gene into the brain cells that need it. Adeno-associated viruses (AAVs) have been the vector of choice for gene therapy. Viruses such as AAV9 can bypass the blood-brain barrier and access the brain. But scientists are still working out how to deliver AAV gene therapies to maximize blood-brain barrier penetrance.

Gene therapies can be injected directly into the brain, but this approach isn't perfect either. An earlier gene therapy that used this approach to deliver neuroprotective nerve growth factor (NGF) into patients with mild to moderate Alzheimer's disease passed safety tests but didn't improve symptoms. Parmar said follow-up work showed the NGF therapy didn't reach cholinergic neurons in the basal forebrain, the brain cells that needed it most. The vector failed to travel well within brain tissue, and the trial didn't use tools that would have helped the clinicians assess whether they had injected the right areas of the brain.

Lexeo has instead delivered its gene therapy into patients' cerebrospinal fluid, which circulates through the spinal cord — a technique that bypasses the blood-brain barrier and improves brain-wide delivery. The injection is a 40-minute outpatient procedure, Townsend said, and will meet their goal to "bathe the brain in the vector."

The new study showing the negative effects of APOE3 opens the door to expanding the target population for these gene therapies, Townsend said.

"If the approach for suppressing E4 [APOE4] works, then there's no reason why there could not be a parallel approach to suppressing E3 [APOE3]," Townsend said.

No silver bullet

Ultimately, gene therapies targeting APOE variants have excited the field because they could potentially benefit a vast number of people.

But no lone treatment is likely to be sufficient, said Dr. Shanshan Wang, an anesthesiologist at the University of California, San Diego. Wang is working on a separate gene therapy that she thinks may help protect damaged neurons. That's because even if APOE does have an outsize role in Alzheimer's risk, it's not the whole story.

"When you think about cancer treatment or any other disease treatment, do you just use one therapy?" Wang said. Cancer treatment has thrived on targeting multiple disease facets simultaneously. "It's always combinatory."

A single gene mutation protects against Alzheimer's disease in people destined to get the disease very young — and now we know why.

The gene mutation affects a protein called reelin that directs brain cells to shred the probable culprits in the disease — toxic amyloid plaques and tau tangles. The mutation makes reelin work much more efficiently, new research reveals.

The finding could point the way towards transformative therapies for the condition, experts said.

"I would never have expected that it would be so protective that it actually negates the effect of a dominant early onset Alzheimer's disease mutation," Dr. Joachim Herz, a neuroscientist at the University of Texas Southwestern Medical Center who was not involved in the new research, told Live Science. "That I would never have in my wildest dreams predicted."

A tale of two genes

Unpacking how the protective mutation worked began with a population that faced the opposite problem: an extraordinarily harmful mutation that accelerates Alzheimer's disease.

For decades, people in the lush valleys near Medellin, Colombia, had faced premature memory loss.

Neurologist Dr. Francisco Lopera grew up in the region. While he was still a medical student, he came across his first case, a 47-year-old man displaying memory symptoms usually seen in elderly people with dementia. Lopera traveled across the region, determined to map where people were facing early memory loss. He ultimately identified thousands of people affected by a rare genetic form of Alzheimer's disease. The condition was autosomal dominant, meaning that anyone carrying at least one copy of the mutated presenilin 1 (PSEN1) gene would, like clockwork, lose their memories in their mid-forties.

Lopera's work in mapping this affected population was invaluable to dementia research, but his most important contribution came just a year before he died in 2024. He co-authored a paper in the journal Nature Medicine that detailed the case of a patient he met in his travels across Colombia. This patient had the PSEN1 gene mutation but lived well into his 60s before developing Alzheimer's. This was the neurological equivalent of a house that stays standing for decades despite cracks in its foundations that should give way.

Lopera discovered that this man's resilient brain was strengthened by another mutation, dubbed COLBOS after the research centers in Colombia and Boston that characterized it.

Improving efficiency

The new research, published in December 2025 in the Journal of the American Chemical Society, has identified exactly how the COLBOS mutation protected the patient's brain for decades.

When the COLBOS variant was first identified in 2023, scientists noted that the mutation altered how a cell signaling protein called reelin functioned. The protein promotes the formation of new connections between brain cells, prevents the toxic tau protein from becoming activated, and prevents amyloid plaques from building up in the brain.

COLBOS altered how reelin binds to another signaling molecule called heparan sulfate, a sugar found on the cell surface of virtually all cell types in humans, including neurons. But how reelin's binding ability affected Alzheimer's progression remained unclear. In the new paper, molecular biologist Chunyu Wang and colleagues at the Rensselaer Polytechnic Institute in New York mapped this process.

Wang's study relied on a technique called surface plasmon resonance, which reveals. how strongly a free-floating molecule — in this case, reelin — binds to a molecule anchored to a sensor surface — in this case, heparan sulfate. Wang's team saw that the COLBOS mutation acted like a molecular glue, strengthening the bonds between the two molecules, suggesting it could cause reelin to accumulate at the surface of neurons in the brain.

This change explained why COLBOS was able to ward off Alzheimer's. When reelin binds to heparan sulfate, the protein becomes localized to the surface of brain cells, where its anti-Alzheimer's signaling is most effective. Here, reelin can more easily ward off cognitive decline by slowing key Alzheimer's disease processes, such as the phosphorylation of the tau protein, said Wang. Phosphorylation destabilizes the normally ordered structure of tau, causing toxic tangles to build up in neurons.

Herz mapped out much of the reelin pathway 20 years ago in a series of papers. Herz's work was in mice, and although his team predicted reelin mutations could be neuroprotective, it was only through Lopera's tireless clinical work that the theory was proven.

Uphill battle

Unfortunately, as Lopera noted, the COLBOS mutation could only delay rather than prevent people with rare Alzheimer's mutations from getting the disease. Herz's theory is that patients with PSEN1 mutations exhibit malfunctions in organelles called the endolysosomal compartments. These are like cellular shredders that chop up troublesome proteins like tau and amyloid. He added that the COLBOS mutation makes the process of feeding these proteins into the shredders more effective.

But as the brain ages, Herz said, the shredder's defects become harder to overcome, despite reelin's effects, leading to Alzheimer’s.

The findings could have useful implications for future Alzheimer's therapies that delay or prevent disease in the vast majority of patients, including ones without high-risk PSEN1 mutations. Wang pointed to recent research that showed reelin-producing neurons are some of the first to die in Alzheimer's disease. Without these neurons, less reelin is made, toxic waste builds up, and Alzheimer's disease accelerates.

Wang hypothesized that if they could get reelin to act more efficiently at brain cell surfaces, even with less reelin present, that could protect such people from further symptoms. Wang is currently discussing with a colleague at Rensselaer the development of a gene therapy that enhances reelin signaling based on these findings.

Wang pointed out that even if researchers could delay Alzheimer’s by a fraction of the two decades that the COLBOS mutation granted to the Colombian patients, it would be by far the biggest disease improvement ever realized with Alzheimer's. Current drugs on the market for the condition may extend independent living by two to three years, tops, he said, so "20 years is amazing."

Brain-training exercises may reduce the risk of dementia if they involve speedy thinking, whereas exercises involving memorization or reasoning have no effect on dementia risk, a two-decade-long trial suggests.

The finding could prompt researchers to design video games to help preserve users' cognitive function as they get older, some experts say.

As people age, their probability of developing Alzheimer's disease or another form of dementia increases, and these conditions affect nearly half of people in their 80s and 90s, Art Kramer, a psychologist at Northeastern University who was not involved with the new study, told Live Science. There is currently no cure for these disorders, but researchers are exploring interventions to reduce the risk of dementia. Some available drugs can help slow cognitive decline in early stages of the disease, but they're far from silver bullets.

Now, a trial that began in the late 1990s is pointing to non-pharmaceutical interventions that might help ward off dementia.

Weeks of training meant years of protection

At the study's start, 2,021 participants ages 65 and older enrolled in the long-term randomized controlled trial, whose results were published Feb. 9 in the journal Alzheimer's & Dementia. These participants were split into four groups. One group performed speed-training exercises, which required them to divide their attention between two tasks at once. The other three groups completed memorization exercises in which they used mnemonics; reasoning exercises that involved spotting patterns and using them to solve problems; or no cognitive exercises at all, as a point of comparison.

Participants in the three training groups completed up to 10 60- to 75-minute-long sessions over five or six weeks. Some participants also returned for up to four 75-minute-long "booster" sessions one to three years later.

Twenty years after the study began, the trial runners determined that only the speed-training exercises were linked to a reduced risk of Alzheimer’s disease and dementia. The effect was more pronounced in the booster group.

"If you were in the speed training group and you had the booster sessions, you had a 25% lower risk of having a diagnosis of dementia [by the end of the trial]," said study co-author Marilyn Albert, a neuroscientist at John Hopkins University. By comparison, dementia was just as common in the other two training groups as it was in the comparison group, suggesting the memory and reasoning tasks had no protective effect.

The trial results raise the question as to whether speed-training cognitive exercises, including certain brain-training video games or apps, could help guard against dementia.

"There are hundreds of those that exist in the marketplace" and claim to be designed to boost brain health, Kramer said. "When these things get commercial, sometimes people make claims that go beyond the data, so you always worry about that," he cautioned. But still, he argued that these games could theoretically achieve a similar effect to the speed-training cognitive exercises tested in the trial.

Albert, meanwhile, is hesitant to suggest that video games could recapitulate the effects seen in this study.

"Speed-of-processing training isn't a whole lot of fun. It's hard," she told Live Science. She argued that the most important factor of the speed-training exercises, which may be missing from video games, was that they were adaptive. They involved looking for objects in the center and at the edges of a computer screen to find two that match; the exercise would refresh faster and with more objects as performance improved.

This adaptation wasn't an element of the memory and reasoning exercises, which may explain why those didn't lead to a significantly reduced risk of dementia, Albert said.

One strength of the trial was that it included a large group of participants, a quarter of whom belonged to minority groups. "People who are Black or Hispanic have a higher risk of dementia," Albert said, arguing that their representation in the study may make the results more generalizable.

The next step is to investigate whether the exercises prompted any specific brain changes that delayed neurodegeneration.

"We need to understand the mechanisms, because if we did, then we could better design the interventions," Albert said. Kramer suggested following up with MRI scans to see how cognitive exercises alter brain anatomy in human participants.

He noted that scientists can train lab animals, such as rodents, to perform similar training exercises. "And then you can do things that are a bit more invasive," he added, such as changing the lab mice's genetic makeup to understand what genetic factors are at play.

In the meantime, scientists already know of other lifestyle factors that are tied to a lower risk of Alzheimer's disease and other forms of dementia, Albert noted. These include engaging in regular physical activity and maintaining blood pressure within the normal range. Someday, perhaps brain-training exercises will also become a common method to stave off dementia — especially since, in the trial, it took only a few weeks of training to protect the participants for 20 years, Albert said.

This article is for informational purposes only and is not meant to offer medical advice.

Over the past two centuries, vaccines have been critical for preventing infectious diseases. The World Health Organization estimates that vaccination prevents between 3 million and 5 million deaths annually from diseases like diphtheria, tetanus, influenza, measles and, more recently, COVID-19.

While there has long been broad scientific consensus that vaccines prevent or mitigate the spread of infections, there is new research suggesting that the therapeutic impact might go beyond the benefit of preventing infectious diseases.

An April 2025 study published in the prominent journal Nature found tantalizing evidence that the herpes zoster — or shingles — vaccine could lower the risk of dementia in the general population by as much as 20%.

We are a team of physician scientists with expertise in the clinical and basic science of neurodegenerative disorders and dementia.

We believe that this study potentially opens the door to other breakthroughs in understanding and treating dementia and other degenerative disorders of the brain.

A role for vaccines in reducing dementia risk?

One of the major challenges researchers face when trying to study the effects of vaccines is finding an unvaccinated "control group" for comparison — a group that is similar to the vaccine group in all respects, save for the fact that they haven't received the active vaccine. That's because it's unethical to assign some patients to the control group and deprive them of vaccine protection against a disease such as shingles.

The Nature study took advantage of a policy change in Wales that went into effect in 2013, stating that people born on or after September 2, 1933, were eligible for the herpes zoster vaccination for at least a year, while those born before that cutoff date were not. The vaccine was administered to prevent shingles, a painful condition caused by the same virus that causes chickenpox, which can lie dormant in the body and be reactivated later in life.

Related: Shingles vaccine may directly guard against dementia, study hints

The researchers used the policy change as a natural laboratory of sorts to study the effect of shingles vaccination on long-term health outcomes. In a statistically sophisticated analysis of health records, the team found that the vaccine reduced the probability of getting dementia by one-fifth over a seven-year period. This means that people who received the shingles vaccine were less likely to develop clinical dementia over the seven-year follow-up period, and women benefited more than men.

The study design allowed researchers to compare two groups without actively depriving any one group of access to vaccination. The two groups were also of comparable age and had similar medical comorbidities — meaning similar rates of other medical conditions such as diabetes or high blood pressure.

Results from this and other related studies raise the possibility that vaccines may have a broader role in experimental therapeutics outside the realm of infectious diseases.

These studies also raise provocative questions about how vaccines work and how our immune system can potentially prevent dementia.

How vaccines might be protective

One scientific explanation for the reduction of dementia by the herpes zoster vaccine could be the direct protection against the shingles virus, which may play a role in exacerbating dementia.

However, there is also the possibility that the vaccine may have conferred protection by activating the immune system and providing "trained immunity," in which the immune system is strengthened by repeated exposure to vaccines or viruses.

The study did not differentiate between different types of dementia, such as dementia due to Alzheimer's disease or dementia due to stroke. Additionally, researchers cannot draw any definitive conclusions about possible mechanisms for how the vaccines could be protective from an analysis of health records alone.

The next step would be a prospective, randomized, double-blind, placebo-controlled study — the "gold standard" for clinical trials in medicine — to directly examine how the herpes zoster vaccine compares with a placebo in their ability to reduce the risk of dementia over time. Such studies are necessary before any vaccines, as well as other potential therapies, can be recommended for routine clinical use in the prevention of dementia.

The challenges of untangling dementia

Dementia is a major noncommunicable disease that is a leading cause of death around the world.

A January 2025 study provided updated figures on lifetime dementia risk across different subsets of the U.S. population. The researchers estimate that the lifetime risk of dementia after age 55 is 42% — more than double earlier estimates. The dementia risk was 4% by age 75, and 20% by age 85, with the majority of risk occurring after 85. The researchers projected that the number of new cases of dementia in the U.S. would double over the next four decades from approximately 514,000 cases in 2020 to 1 million in 2060.

Once considered a disease largely confined to the developed world, the deleterious effects of dementia are now apparent throughout the globe, as life expectancy increases in many formerly developing countries. While there are different forms of dementia with varying clinical manifestations and underlying neurobiology, Alzheimer's disease is the most common.

Prospective studies that specifically test how giving a vaccine changes the risk for future dementia may benefit from studying patient populations with specific types of dementia because each version of dementia might require distinct treatments.

Unfortunately, for the past two to three decades, the amyloid hypothesis of Alzheimer's disease — which posits that accumulation of a protein called amyloid in the brain contributes to the disorder — dominated the scientific conversation. As a result, most of the efforts in the experimental therapeutics of Alzheimer's disease have focused on drugs that lower the levels of amyloid in the brain.

However, results to date have been modest and disappointing. The two recently approved amyloid-lowering therapies have only a minimal impact on slowing the decline, are expensive and have potentially serious side effects. And no drug currently approved by the Food and Drug Administration for clinical use reverses the cognitive decline.

Studies based on health records suggest that past exposure to viruses increase the risk of dementia, while routine vaccines, including those against tetanus, diphtheria, pertussis, pneumonia, shingles and others, reduce the risk.

Innovation and an open mind

There is sometimes a tendency among scientists to cling to older, familiar models of disease and a reluctance to move in more unconventional directions.

Yet the process of doing science has a way of teaching researchers like us humility, opening our minds to new information, learning from our mistakes and going where that data takes us in our quest for effective, lifesaving therapies.

Vaccines may be one of those paths less traveled. It is an exciting possibility that may open the door to other breakthroughs in understanding and treating degenerative disorders of the brain.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

The U.S. Food and Drug Administration (FDA) recently cleared a blood test that detects signs of Alzheimer's disease in the brain, according to multiple studies. This is the first-ever blood test available for this common form of dementia.

Here's how the new blood test works and why it could be useful to patients.

Could the blood test advance Alzheimer's research?

The test will give researchers a more precise idea of how a patient's clinical symptoms relate to the findings on their blood test, Azizi said. "It's a great way of using a biomarker [measurable sign of disease] in the blood to make an earlier diagnosis to give a drug" to slow disease progression, he said.

Azizi added that this blood test could help track whether a treatment for Alzheimer's disease is working, which would be useful both for patients receiving approved medicines and those in trials of new drugs. Looking forward, researchers will also be able to evaluate how well blood-based testing works in more diverse populations, Day noted.

This article is for informational purposes only and is not meant to offer medical advice.

The shingles vaccine may prevent or delay dementia, compelling new data suggest.

In a study published April 23 in the journal JAMA, researchers analyzed electronic health records from across Australia. They found that older adults who were eligible for a free shingles vaccine were significantly less likely to be diagnosed with dementia over the following 7.4 years than those who were slightly too old to qualify for the vaccination program.

These findings support the "viral hypothesis" of Alzheimer's disease, which posits that viral infections contribute to the development of the condition, which is the most common form of dementia. Specifically, the hypothesis points to herpesviruses, a family of viruses that includes varicella-zoster virus, the germ behind chickenpox and shingles.

If confirmed by additional research, the results of the new study suggest that an effective and low-cost tool for reducing dementia risk may already exist.

Related: 'Reanimated' herpes viruses lurking in the brain may link concussions and dementia

"It is very hard to see how anything other than the vaccine could explain the strong protective effect" observed in the study, Dr. Sten Vermund, dean of the University of South Florida College of Public Health, who was not involved in the work, told Live Science in an email.

A pseudo-clinical trial

If a person contracts chickenpox, the varicella-zoster virus can remain dormant in the nervous system for decades before reactivating later to cause shingles, a condition marked by a painful rash. The ability to fall latent and then "reawaken" in the body is a core characteristic of herpesviruses.

The shingles vaccine helps to build immunity and prevent reactivation of the virus, and it's thus highly effective at preventing shingles and its complications, such as long-term nerve pain, vision loss and a higher risk of bacterial skin infections.

Previous studies found that older people who have been vaccinated against shingles tend to have lower rates of dementia than those who have not received the shingles vaccine. But these studies had a major caveat: People who choose to get vaccinated also tend to be more health-conscious and more likely to eat well and exercise regularly — habits that also help protect against dementia. So, while past research showed a correlation between shingles vaccination and reduced dementia risk, it couldn't prove that one caused the other.

The gold-standard test to see whether the vaccine actually protects against dementia would be to conduct a large clinical trial, in which participants would be randomly assigned to receive the vaccine or a placebo. But such trials are costly, and in this case, could potentially pose ethical issues.

"It would be nice to see a randomized and controlled study, showing placebo versus herpes vaccine, rather than a retrospective observational as this study was," said Dr. Logan DuBose, co-founder of Olera.care, a caregiver support platform for senior care needs. "However, there might be some ethical issues with giving some people the vaccine and others not" — given it's known to be effective against shingles — "making that a hard study to conduct," DuBose, who was not involved in the work, told Live Science in an email.

The new study took a different approach. "What's so special about our study is that we take advantage of a very similar scenario to a randomized trial," senior author Dr. Pascal Geldsetzer, an assistant professor of medicine at Stanford University, told Live Science in an email.

Australia launched a shingles vaccination program on Nov. 1, 2016, providing a unique opportunity for a quasi-experimental study. The program offered a free shingles vaccine to adults ages 70 to 79. Those who turned 80 just before the program began were ineligible, while those who turned 80 just afterward were eligible.

As in a clinical trial, "we have a vaccine-eligible and a vaccine-ineligible group for which we know that they should be on average similar to each other, and therefore good comparison groups," Geldsetzer said. "All that's different about these two groups is if they were born a few days earlier or a few days later."

Related: Why do we develop lifelong immunity to some diseases, but not others?

A decrease in dementia risk

The researchers analyzed data from over 101,200 individuals across 65 general medical practices in Australia, focusing on those born just before and after Nov. 2, 1936 — the cutoff birthday for vaccine-program eligibility. The difference in vaccination rates between these two cohorts was substantial, with eligibility boosting the likelihood of receiving the vaccine.

Over a 7.4-year follow-up period, the rate of dementia among eligible individuals was 1.8 percentage points lower than that of ineligible people. Overall, 3.7% of the eligible individuals were diagnosed with dementia, compared to 5.5% of ineligible individuals.

This effect was not observed for other chronic conditions, such as high blood pressure, heart disease or diabetes, suggesting that the shingles vaccine had a specific protective effect against dementia. The analysis also showed no increase in diagnoses of other common chronic conditions, or use of other preventive services — like cancer screening or annual flu vaccination — among those who were vaccine-eligible. This reinforced the idea that the difference in dementia was driven by the vaccine itself.

Previously, Geldsetzer and his team conducted a similar analysis of health records in Wales and found that the shingles vaccine was linked to a 20% lower rate of new dementia diagnoses among vaccinated individuals.

"My first thought [about the Australian study] was that there is a modest difference, being 1.8% less likely to get a diagnosis," DuBose said. However, having two well-designed studies that show the risk of dementia diagnosis is lower if you've had the vaccination is compelling, he said.

Limitations and next steps

DuBose noted that the study could have gone a step further by examining whether the vaccine's effect differed in people with different genetic backgrounds. For instance, a specific gene variant called APOE4 is linked to dementia. It could be that the vaccine's effects vary depending on a person's genetic background, he suggested.

More studies are needed to understand the mechanism behind the vaccine's protective effect against dementia, as that's currently unclear. One theory suggests that reactivation of the varicella-zoster virus may trigger brain damage through a range of mechanisms, including the buildup of abnormal proteins and chronic inflammation. By preventing reactivation, the shingles vaccine may theoretically prevent this brain damage.

Another hypothesis is that the vaccine provides protection not by targeting viruses directly but by tuning the immune system in a way that slows or alters the course of dementia.

Now, Geldsetzer and his team are seeking private and philanthropic funding to launch a formal clinical trial testing the shingles vaccine's ability to protect against dementia.

This article is for informational purposes only and is not meant to offer medical advice.

A man whose genetics almost guaranteed that he would develop Alzheimer's disease by his 50s has somehow made it to his mid-70s with nary a symptom.

The now-75-year-old man, Doug Whitney, is one of only three people known to have escaped their genetic fate, sidestepping a rare form of Alzheimer's disease called dominantly inherited Alzheimer's disease (DIAD). Caused by several gene mutations, DIAD makes up less than 1% of all Alzheimer's cases, and its symptoms typically set in between ages 35 and 55.

A new study, published Feb. 10 in the journal Nature Medicine, details Whitney's case and pinpoints potential factors that may have shielded him from the neurodegenerative disorder thus far. One hypothesis is that his exposure to very high heat as a shipboard mechanic could have somehow contributed to this resilience, co-lead author Dr. Jorge Llibre-Guerra, an assistant professor of neurology at the Washington University School of Medicine in St. Louis and co-first author of the study, told Live Science.

This report adds to the handful of cases that are "potentially, a critical source for understanding molecular mechanisms that can slow or stave off Alzheimer's disease pathogenesis," Dr. Michael Greicius, an Alzheimer's researcher at Stanford University who was not involved in the study, told Live Science in an email.

Related: A man's rare gene variant may have shielded him from devastating form of early Alzheimer's

A "shocking" surprise

Whitney told the research team that he thought he was one of the few who had escaped the mutations that had caused so much DIAD in his family. At age 61 — when Whitney first approached the researchers about enrolling in a large trial about DIAD — he showed no signs of Alzheimer's disease, whereas his mother and 11 of her 13 siblings had developed the condition by the time they were in their 50s.

DIAD is caused by mutations in three genes: amyloid precursor protein (APP), presenilin-1 (PSEN1) or presenilin-2 (PSEN2). The overwhelming majority of people with DIAD only carry one of these mutations, although Llibre-Guerra said he's come across a few who carried more than one.

"Once you inherit some of these mutations, you have like a 99.99% chance of developing the disease," Llibre-Guerra said. That's why Whitney was "shocked" to discover that he carried a mutation in the PSEN2 gene that should have led to early-onset Alzheimer's, he added.

Now, at 75, Whitney still hasn't developed symptoms of the condition, which makes him one of three people known to have escaped near-certain DIAD, per the study.

To understand Whitney's apparent protection, Llibre and his colleagues used brain scans to look for the telltale signs of Alzheimer's — namely, abnormal protein clumps called amyloid-beta plaques and tau protein tangles.

The accumulation of amyloid-beta plaques is an early step in the development of Alzheimer's disease, followed by an accumulation of "tangles" of tau protein. Evidence suggests the interplay between these two proteins is potentially what leads to cognitive decline, although these may not be the only factors at play.

Whitney's brain turned out to be flooded with amyloid, but unlike in other DIAD patients, the tau had stayed contained within a small section of the brain. These tangles were at the back of his skull, in his left occipital lobe.

This pattern adds weight to the idea that "if we prevent the downstream effects of amyloid-beta, we might delay the onset of the disease," Llibre-Guerra said. In other words, it seems like the chain reaction between amyloid and tau was somehow broken in Whitney's brain. "The question that we have is, what is preventing tau spread in this particular case?" he added.

This observation echoes what had previously been seen in another DIAD "escapee" who also had a mutation in the PSEN1 gene, Jean-Charles Lambert, an Alzheimer's researcher from the Inserm Institute at the University of Lille who was not involved in the study, told Live Science in an email.

Could extreme heat have been protective?

A few gene variants are known to protect against Alzheimer's. One example is the so-called E2 allele of the APOE gene, which is associated with a very low risk of developing the disease, Lambert said.

But the team did not find any of these known variants in Whitney's genetic makeup. Instead, they pinpointed several other variants that could be interesting to study in the context of Alzheimer's. These include one variant spotted in GPCPD1, a gene recently linked to Alzheimer's resilience. Another variant, found in the CD33 gene, could warrant further research, Llibre-Guerra said, as it's involved in immune responses in the brain.

The scientists also found higher-than-normal levels of "heat-shock proteins" in Whitney's cerebral spinal fluid, the liquid that cushions the brain and spinal cord. Heat-shock proteins help protect the body from environmental stresses, such as extreme heat, and could be linked to Whitney's time working as a shipboard mechanic in boiling engine rooms, the team suggested.

"We know that these proteins are involved in preventing misfolding proteins in the brain," Llibre-Guerra said. Like origami, proteins must be folded in a particular way to work, and Alzheimer's is a disease in which this folding goes awry. "Maybe it's preventing more tau from being misfolded and spreading," Llibre-Guerra suggested, adding that this is "just a hypothesis" at this stage.

For Lambert, this explanation is "highly speculative," as the evidence to support it is still very tentative. Greicius added that there are "countless other possible explanations" for Whitney's resilience against Alzheimer's, although this is an "interesting and plausible hypothesis."

The team's genetic investigation was a "reasonable first analysis," but it could have left "thousands of potentially protective variants unexamined on the cutting-room floor," Greicius added. And because this was a case study of only one person, it's challenging to identify a genetic variant or environmental exposure that may have helped him, he said.

Still, Greicius said, studies like this one are "useful for generating novel hypotheses."

This article is for informational purposes only and is not meant to offer medical advice.

Inflammation can reawaken dormant viruses in the brain, which may help to explain why concussions often precede dementia, a new study finds.

Brain injuries like concussions raise the risk of dementia, and the more blows someone takes to the head, the higher that risk becomes, evidence suggests. Scientists are investigating what happens in the brain after injury that might lead to changes tied to dementia — for instance, a buildup of abnormal proteins and the malfunction and death of brain cells. Such changes are seen in Alzheimer's disease and chronic traumatic encephalopathy (CTE), a disorder that's recently gained recognition in high-impact sports.

Some scientists think these changes may be linked to a common virus: herpes simplex virus 1 (HSV-1), the germ behind cold sores.

Herpesviruses — a broader group that also includes the viruses behind chickenpox and mono — have an ability to go dormant in the body and then later reactivate. "They can remain latent in your body forever," said lead study author Dana Cairns, a postdoctoral research fellow at Tufts University. There's evidence that HSV-1 can somehow weasel its way into the brain and then lie there in wait, Cairns told Live Science.

Related: Lab-grown 'minibrains' help reveal why traumatic brain injury raises dementia risk

What's new here is that the researchers have demonstrated that physical injury can activate latent viruses in the brain, said Dr. Gorazd Stokin, who leads a neuroscience lab at the Institute of Molecular and Translational Medicine in the Czech Republic and was not involved in the new study.

The new research relied on miniature laboratory models of the brain, so more work will be needed to show that the results are relevant to people. "But it's a good first step to show something interesting," said Stokin, who is also a consultant neurologist at the Gloucestershire Hospitals NHS Foundation Trust in the U.K.

Viruses in dementia

The idea of viruses sparking dementia isn't new; Ruth Itzhaki, a co-author of the new paper, raised the notion in 1991. Itzhaki and colleagues had found the virus in the brains of older adults who had died of Alzheimer's. They later found that people who carry both the virus and ApoE4 — a gene variant that raises Alzheimer's risk — have a higher risk of the disease than those with ApoE4 alone. They also found that latent HSV-1 can be reawakened by stress or immunosuppression.

"In those days, she got a lot of pushback," Cairns said of Itzhaki's early work. This viral theory of dementia remained niche for decades, but in recent years, interest has increased. Nowadays, scientists also have better tools to test the theory, including lab-grown models of the human brain.

The new research, published Tuesday (Jan. 7) in the journal Science Advances, used brain models measuring only 0.2 inches (6 millimeters) across. The spongy, doughnut-shaped structures are made of silk and imbued with stem cells. With specific chemicals, the stem cells are made to mature into various brain cells that carry one copy of ApoE4. This genetic trait is "relatively common" among people with Alzheimer's, Stokin noted, so it's relevant to include in a brain model.

The researchers infected these models with HSV-1 and then pushed the virus into dormancy with an antiviral drug. In past research, they had shown that inflammation could "wake up" the virus and that this triggered brain-cell changes also seen in dementia. In that previous work, the researchers triggered the inflammation with varicella-zoster virus, the virus behind chickenpox and shingles.

But "there are other things besides infection that cause inflammation, like injury," Cairns said. "We wanted to understand if maybe injury could be doing something similar."

In the new study, the team subjected the minibrains to models of two types of injury: severe injury, as if the skull had broken open, and concussions, in which the brain moves or twists in the skull. In the concussion experiments, the minibrains were placed in 3D-printed containers filled with fluid, similar to the fluid that cushions the brain inside the skull. The encased minibrains were then put on a platform that was struck with a piston.

In both experiments, the brain models became inflamed and the HSV-1 in them reactivated. Dementia-related changes, like an accumulation of proteins, showed up in these infected brain models, but not in injured-but-uninfected models that were used for comparison.

The severe-injury experiment damaged the cells so badly that they soon died, but the cells in the concussion experiment survived and thus the experiment could be repeated. The more times it was repeated, the worse the dementia-like pathology of the infected models became.

"The people that are exposed to more chronic injuries over time often clinically have the worst manifestations of neurodegeneration," Cairns noted. "It [the experiment] really correlated very well with that concept."

Additional experiments by the team hinted that blocking inflammation after injury could help stop HSV-1 from reactivating and thus prevent the signs of dementia from arising. This finding strengthened the team's overall results, Stokin said. However, because the results have been shown in only minibrains, "trying to do the same in animal models would be useful," he added.

The researchers plan to continue experimenting with their brain models to see what might stop HSV-1 from reawakening — for instance, anti-inflammatory or antiviral drugs may work, Cairns said.

"If you can block reactivation, or somehow control the viral load … that would be beneficial," Stokin said, assuming herpes truly is a missing link between brain injury and dementia.

Nearly half of all dementia cases could be delayed or prevented altogether by addressing 14 possible risk factors, including vision loss and high cholesterol.

That is the key finding of a new study that we and our colleagues published in the journal The Lancet.

Dementia, a rapidly increasing global challenge, affects an estimated 57 million worldwide, and this number is expected to increase to 153 million by 2050 worldwide. Although the prevalence of dementia is on the decline in high-income countries, it continues to increase in low- and middle-income countries.

This third updated report of the Lancet Commission on Dementia offers good news and a strong message: Policymakers, clinicians, individuals and families can be ambitious about prevention and reduce dementia risk; and for those living with dementia and their caregivers, support their quality of life using evidence-based approaches.

The new report confirms 12 previously identified potentially modifiable risk factors from two previous reports, published in 2017 and 2020. It also offers new evidence supporting two additional modifiable risk factors: vision loss and high levels of low-density lipoprotein (LDL) cholesterol, often called “bad” cholesterol.

Our study of published evidence found that collectively, addressing 14 modifiable risk factors could potentially reduce the prevalence of dementia by 45% worldwide. Even greater risk reductions could be possible in low- and middle-income countries and for people with low income in higher-income countries given the higher prevalence of dementia, health disparities and risk factors in these populations.

The report further indicates that reducing these 14 risks can increase the number of healthy years of life and reduce the length of time with poor health in people with dementia.

RELATED: Gene variant carried by 1 in 5 people may guard against Alzheimer's and Parkinson's, massive study finds

Additionally, the report cites clinical trials showing that nonpharmacological approaches, such as using activities tailored to interests and abilities, can reduce dementia-related symptoms and improve quality of life.

We are a general internist and an applied sociologist and intervention scientist, and our work focuses on memory and wellness in older adults. Together with 25 other internationally recognized dementia experts under the leadership of psychiatry professor Dr. Gill Livingston, we carefully reviewed the evidence to derive recommendations for prevention, intervention and care.

Why it matters

The rapid growth of aging populations worldwide is a triumph of better public and personal health throughout the entire life span. Yet, given the lack of a dementia cure, this report highlights the importance of prevention as well as supporting quality of life for those with a dementia diagnosis.

In the new report, our team proposed an ambitious program for preventing dementia that could be implemented at the individual, community and policy levels and across the life span from early life through mid and late life. The key points include:

• In early life, improving general education.
• In midlife, addressing hearing loss, high LDL cholesterol, depression, traumatic brain injury, physical inactivity, diabetes, smoking, hypertension, obesity and excessive alcohol.
• In later life, reducing social isolation, air pollution and vision loss.

Together, these add up to the Lancet Commission on Dementia’s estimate that 45% of dementia risk can be reduced. And an abundance of new research shows that when risk factors are addressed, such as exposure to air pollution, they are linked with improved cognition and likely reduction of dementia risk.

New evidence supports the notion that in high-income countries, reducing dementia risk can translate to more healthy years, years free of dementia and a shorter duration of ill health for people who develop dementia.

What still isn’t known

The 45% reduction in dementia risk across the world’s population is based on a calculation that assumes that risk factors are causal and can be eliminated. It shows how dementia prevention is critical and the impact it would have on individuals and families.

The commission emphasized the need for more research to identify additional risk factors, test risk factor changes in clinical trials, provide guidance for public health efforts, and identify and evaluate strategies for implementing and scaling evidence-based programs that support people with dementia and caregivers.

The updated report has worldwide public health and research impact and is being widely disseminated. It serves as a guideline to clinicians and policymakers and outlines new research directions.

The Research Brief is a short take on interesting academic work.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Different versions of RNA encoded by single genes may play a role in Alzeimer's disease, new research suggests. These genetic molecules could point to new treatments and ways to spot the disease before its symptoms set in, scientists hope.

The new study, published Wednesday (May 22) in the journal Nature Biotechnology, zooms in on RNA, a cousin of DNA. Among other functions, RNA copies instructions from DNA and relays them to a cell's protein builders. Through a process called "alternative splicing," though, one gene can give rise to many versions of RNA, called isoforms, which in turn may play very different — or even opposite — roles in cell function. 

This is possible because genes are made up of building blocks called exons and introns. The exons contain the important instructions for making proteins, and to make RNA, cellular machinery typically "splices" out the introns, leaving only exons behind. But alternative splicing opens the door to new possibilities — the cell might cut out some exons along with the introns, or perhaps leave a few introns in the final RNA molecule. The mastermind behind this snipping process is known as the spliceosome, and its splicing is directed by various molecules in the cell. 

Thus, thanks to the spliceosome, one gene can make many RNA, although "most genes only express a single isoform," said senior study author Mark Ebbert, a principal investigator and assistant professor at the University of Kentucky College of Medicine. "There's a large proportion that have multiple, but there are some that have a wild number," occasionally in the tens or hundreds.

Related: Scientists just discovered a new way cells control their genes — it's called 'backtracking'

In their new study of human brain tissue, Ebbert and his colleagues uncovered 700 RNA isoforms that had never been described before. And they found that the levels of nearly 100 of these isoforms differed in the brains of people with and without Alzheimer's. 

Notably, the genes behind these isoforms were equally active in both groups of people. This suggests that if scientists only look at a gene's overall activity but not at the different RNAs it's making, they miss out on this nuance. 

"Part of what we're trying to highlight is, look at all this we don't understand," Ebbert told Live Science.

For the study, the team analyzed brain tissue from 12 deceased organ donors who were between 75 and 90 years old when they died; six of the donors had Alzheimer's disease while six had no cognitive impairment. The researchers used a technique called "long-read sequencing" to take a snapshot of RNA present in the brain tissue.

Isoforms born from the same gene tend to be "very similar to each other," said co-first author Bernardo Heberle, a doctoral candidate in Ebbert's lab. So if you analyze only a short snippet of each RNA, "you really can't tell if the fragment came from isoform A, B or C," Heberle told Live Science. Long-read sequencing, as its name suggests, looks at long strings of RNA, enabling researchers to capture differences in the isoforms that might be missed in shorter reads. 

Of the 700 newfound isoforms, 430 could be connected back to known genes, and of those, 53 came from genes that had been tied to health conditions in previous studies. Notably, two genes related to the abnormal amyloid and tau proteins seen in Alzheimer's — APP and MAPT — respectively gave rise to five and four isoforms. 

Related: Alzheimer's is transmissible in extremely rare scenarios

A few isoforms stood out when the team compared the brains of the Alzheimer's patients to those without the disease. For example, a gene called TNFSF12 made two distinct isoforms, the first of which was boosted in the brains of people with Alzheimer's and the second of which was higher in healthy brains. In the past, the TNFSF12 gene has been tied to the brain inflammation seen in Alzheimer's disease — but because the gene makes multiple isoforms, more work may be needed to reveal which one is actually behind this inflammation.  

However, because the recent study included only 12 brains, it's too soon to know if these results carry over to others with and without Alzheimer's, the researchers stressed.

To expand their data set and see which results do carry over, co-first author Ja Brandon, a research assistant professor at the University of Kentucky College of Medicine, is now leading an effort to conduct the same study with more than 300 brains. In the long run, the researchers hope certain RNA isoforms may be prime targets for future Alzheimer's drugs. 

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website! 

A new, large observational study has freshly stoked the debate as to whether taking sildenafil, the active ingredient in the erectile-dysfunction drug Viagra, can help ward off Alzheimer's disease. 

The study included an analysis of insurance claims data from more than 2 million patients with pulmonary arterial hypertension, a form of high blood pressure in the lungs. It revealed that people who took sildenafil — which is used to treat this condition under the brand name Revatio — had a 30% to 54% lower risk of developing Alzheimer's, compared with patients who took four other types of blood-pressure drugs. 

In separate lab experiments, the researchers grew neurons from stem cells donated by patients with Alzheimer's and exposed them to sildenafil for five days. Following treatment, the team measured the cells' levels of phosphorylated tau, a protein that accumulates in the brains of people with Alzheimer's and is believed to partially drive the disease. They found that the tau levels fell steadily as the amount of sildenafil increased. 

The sildenafil-treated neurons also switched on genes tied to nerve growth and reduced inflammation. In their new paper, published March 19 in the Journal of Alzheimer's Disease, the scientists concluded that sildenafil could be a "potential repurposable drug" for this form of dementia. 

But according to the researchers and other experts, more research is warranted.

Related: Alzheimer's may be caused by immune cells thinking brain cells are bacteria, expert says

Over the past two decades, numerous animal studies and observational studies in humans have demonstrated this potential link between the little blue pill and Alzheimer's disease risk. However, the jury is still very much out on whether and how it works. 

Scientists don't yet understand the physiological mechanism by which sildenafil could impact brain disorders like Alzheimer's, but several suggestions have been made. For example, sildenafil works by relaxing blood vessels and increasing blood flow by inhibiting an enzyme called phosphodiesterase 5. In the case of Viagra, this helps users maintain penile erections, whereas for Revatio users, it helps to lower blood pressure. In theory, sildenafil might somehow increase blood flow to the brain and thus help clear proteins associated with Alzheimer's, such as phosphorylated tau. 

However, other observational research in humans has put a damper on this idea, hinting that these kinds of drugs may not have any effect on the disease. 

"While sildenafil can reach the brain, it is questionable if the dose taken and the time course over which the drug was taken can impact on long term changes in brain function that lead to Alzheimer's," Mark Dallas, an associate professor in cellular neuroscience at the University of Reading in the U.K. who was not involved in the research, told Live Science in an email. 

Aspects of how the recent Journal of Alzheimer's Disease study was conducted also cast doubt on the findings. 

For example, although the authors tried to account for some factors that could influence the development of Alzheimer's — such as sex, age and comorbidities — they didn't consider factors like genetics and socioeconomic status. This may have biased their findings. The authors also treated the neurons in the lab with really high, and potentially unrealistic, doses of sildenafil that were around 1,000 times greater than the amount thought to be able to reach the brain.

Definitively proving that taking sildenafil reduces the risk of Alzheimer's disease will require large, clinical trials that include a control group that is appropriately matched to treated individuals in terms of age, sex and medical history. This will allow scientists to paint a clearer picture of the true, potential brain-protecting effects of the drug, as well as any potential side effects it may have. 

"The idea of repurposing drugs for dementia is tantalizing," Dallas said. "However there is a need to carry out well designed clinical trials to provide the robust evidence base needed to add sildenafil to drugs that can manage Alzheimer's disease." 

This article is for informational purposes only and is not meant to offer medical advice. 

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For the first time, scientists have identified people with Alzheimer's whose disease was likely triggered by a medical treatment — one that's now been banned for decades. 

Alzheimer's is caused partly by the gradual accumulation of amyloid-beta and tau proteins in the brain, which trigger a cascade of events that lead to the death of brain cells. Now, a new study provides what may be the first clinical evidence that the "seeds" of these proteins can be extracted from one person and planted into another, sparking disease. However, this seed transfer occurred in a very specific and extraordinary medical context. 

"This is not transmissible in the sense of a viral or bacterial infection," Dr. John Collinge, co-senior study author and a professor of neurology at University College London, said during a Jan. 25 news conference. 

"You can't catch Alzheimer's disease by living with somebody with Alzheimer's, being a carer or a health care worker," because the "seeds" of the disease can't be transmitted that way, he emphasized.

Related: Alzheimer's comes in at least 5 distinct forms, study reveals

In the new study, published Monday (Jan. 29) in the journal Nature Medicine, researchers studied eight people in the U.K. who, as children, received a medical treatment that's now banned in many countries. Between 1959 and 1985, they received human growth hormone (hGH) that had been extracted from the brains of human cadavers. 

This procedure was used to treat growth hormone deficiency —  especially in the U.K., the U.S. and France — before it was banned in many countries in the 1980s. It was then replaced by synthetic versions of hGH. 

The cadaver-sourced hormone was ultimately banned because patients had begun dying from Creutzfeldt-Jakob disease (CJD) — a so-called prion disease that triggers an accumulation of abnormal proteins in the brain. Perhaps the most famous prion disease affects cattle and is known as "mad cow disease," or bovine spongiform encephalopathy. 

Prions are proteins that act like "seeds" of disease, causing healthy proteins to fold in abnormal, harmful ways. The prions group together and form long fibers that eventually become plaques, similar to how amyloid-beta and tau propagate and grow in the brain in Alzheimer's. 

In previous work, the researchers had analyzed the brains of people who died of CJD after receiving cadaver-sourced hGH. In addition to the markings of CJD, they had amyloid-beta pathology in their brains. However, because they died relatively young, it was unclear if they'd developed symptoms of Alzheimer's, or if these would have been masked by those of CJD. 

Separate postmortem analyses of patients who received cadaver-sourced hGH also suggested that Alzheimer's could be spread this way, but until now, this hadn't been confirmed in living people, the authors wrote in the paper. 

Related: Brain inflammation may drive mood changes in Alzheimer's

In the new study, the authors clinically assessed eight recipients of cadaver-sourced hGH who never developed CJD. Five of the eight patients had signs of early-onset dementia, with symptoms beginning between age 38 and 55. The team also analyzed proteins in the clear liquid that surrounds the patients' brains and spinal cords, and they found further evidence to support the diagnosis of Alzheimer's in two patients. 

In addition, the team screened brain tissue samples from one patient who died during the study and detected signs of Alzheimer's pathology. Genetic testing ruled out the possibility that genes associated with early-onset Alzheimer's had caused any of the patients' dementia, although this data was unavailable for two of the patients. 

Other variables, such as the illnesses for which the patients originally needed the hGH, may have influenced their Alzheimer's risk, the study authors noted. However, their only unifying risk factor was their childhood hGH treatment, Dr. Gargi Banerjee, lead study author and a clinical lecturer at University College London, said during the news conference.

The most common form of Alzheimer's is the sporadic version that affects 90% of patients and usually emerges after age 60 — there's no reason to think that this common form of the disease ever originates from clinical procedures, David Westaway, science programs director at the Institute for Neurodegenerative Diseases at the University of California, San Francisco, who was not involved in the research, told Live Science in an email. 

Nonetheless, the study does suggest that, in very rare cases, Alzheimer's can spread in a similar way to a prion disease. In theory, accidental transmissions of Alzheimer's "seeds" could be possible in other medical procedures, so the study authors recommended that steps be taken to prevent that possibility, they wrote in the paper. 

This article is for informational purposes only and is not meant to offer medical advice. 

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Extreme mood changes associated with Alzheimer's disease may be partially driven by brain inflammation, new research suggests. 

Historically, the prevailing theory for what causes Alzheimer's disease was that a gradual buildup of abnormal proteins called amyloid-beta and tau in the brain triggers a cascade of events, leading to nerve damage, the death of brain cells, and symptoms of cognitive decline and mood problems. 

However, emerging evidence suggests that inflammation in the brain may also be involved in the development of the disease. Specific culprits include immune cells called microglia, which normally promote inflammation in response to injury or disease. Activated microglia have been found to interact with amyloid-beta and tau proteins and may influence the progression of Alzheimer's disease. 

And now, in a study published Nov. 27 in the journal JAMA Network Open, scientists have provided what they say is the first strong evidence that the neuropsychiatric symptoms of Alzheimer's are directly associated with microglia activation. 

Better understanding the role inflammation plays in the development of Alzheimer's could take us one step closer to developing more targeted treatments for the disease, the researchers say. 

Related: Gene variant carried by 1 in 5 people may guard against Alzheimer's and Parkinson's, massive study finds

"Neuropsychiatric symptoms such as irritability, agitation, anxiety and depression are among the most difficult symptoms to treat in patients with Alzheimer's," Dr. Cristiano Aguzzoli, the study's lead author and a postdoctoral researcher at the University of Pittsburgh, said in a statement. 

"Here, we show for the first time that brain inflammation may be to blame for these symptoms," he said. 

In the new study, the authors recruited 70 people who had no symptoms of cognitive decline and 39 who were cognitively impaired, either displaying early signs of memory loss known as mild cognitive impairment or dementia caused by Alzheimer's. The participants ranged from age 38 to 87. 

The authors assessed whether the participants displayed any of the mood problems that are characteristic of Alzheimer's. The researchers also scanned the participants' brains to look for signs of microglial activation, as well as the accumulation of amyloid-beta and tau proteins. 

People with cognitive impairment were more likely to have amyloid-beta and tau proteins in their brains. For example, amyloid-beta was found in 79% of those with cognitive impairment compared to 30% without. 

However, even after taking these factors into account, the participants with more severe neuropsychiatric symptoms had a greater level of microglial activation and more substantial signs of inflammation than the participants with milder symptoms. This inflammation specifically affected three regions of the outer layer of the brain. Of the mood symptoms, irritability was most strongly associated with microglial activation, followed by nighttime disturbances and agitation. 

The authors didn't directly compare whether participants' protein buildup was more or less strongly associated with mood problems than their inflammation levels. So they couldn't determine whether one factor is more influential than the other. However, the researchers think it's possible that both are playing a role. 

In addition to conducting these tests, the researchers asked the caregivers of the patients with cognitive decline to fill out a questionnaire about their experiences. They found that the caregivers were more likely to report distress when looking after participants with greater levels of brain inflammation, particularly when it was linked to symptoms of irritability. Caregivers were also more likely to report that patients experienced rapid mood swings when the patients had high inflammation levels. 

Going forward, the authors want to conduct more studies with larger groups of patients, including those who are at later stages of the disease and experience more extreme neuropsychiatric symptoms, such as hallucinations or delusions. This would assess whether the team's findings are more generalizable to the wider population of people with Alzheimer's. 

In the meantime, they hope this research will act as a springboard for developing new therapies for Alzheimer's and possibly other types of dementia. 

"Since both neuroinflammation and neuropsychological abnormalities are found in several other types of dementia, including Parkinson’s dementia, we are collaborating with scientists around the world to expand these findings to these other diseases," Dr. Tharick Pascoal, co-senior study author and an associate professor of psychiatry and neurology at the University of Pittsburgh, said in the statement. 

This article is for informational purposes only and is not meant to offer medical advice.

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The MIND diet — which is intended to guard against dementia, and is rich in fruits and veggies and low in saturated fats — has no short-term brain benefits beyond those seen in people who follow a standard, "suboptimal" diet, a three-year trial suggests.

The trial's results, published Tuesday (July 18) in The New England Journal of Medicine, showed that participants who followed the MIND diet for three years showed slight improvements in their overall cognition, as measured with a dozen tests. However, those mental improvements were not statistically different from those seen in people who followed their usual diets. 

A subset of people from both the MIND and standard diet groups also underwent brain scans, which revealed that their brains changed in the same ways over the three-year period, regardless of the diet they followed. 

"We really expected that the MIND diet would show an effect above the control group, so we were quite surprised by the outcome," Lisa Barnes, lead study author and an associate director of the Alzheimer's Disease Center at Rush University Medical Center in Chicago, told CNN.

Related: Does the Mediterranean diet reduce dementia risk? 20-year study hints no 

The MIND diet, short for "Mediterranean-DASH Intervention for Neurodegenerative Delay" diet, is essentially a mash-up of two other diets hypothesized to improve brain health and reduce the risk of dementia. The broadly defined Mediterranean diet is rich in vegetables, whole grains, legumes, seafood and unsaturated fats like olive oils and low in red meat, eggs, saturated fats and sweets. The Dietary Approaches to Stop Hypertension (DASH) diet is very similar but offers specific daily and weekly nutrition goals and limitations on salt intake.

Large observational studies have linked the MIND diet to a lower rate of Alzheimer's disease and an overall slower rate of cognitive decline in older adults, according to the National Institute on Aging. However, few gold-standard clinical trials have examined this link, and the biological reasons why the MIND diet might have this protective effect have not been clearly demonstrated in humans.

The new trial included 604 adults ages 65 and older who, at the start of the trial, were cognitively healthy but had a family history of dementia. All of the study participants were also overweight and followed "suboptimal" diets, meaning diets that significantly diverged from the MIND diet, at the start of the trial.

The participants were split into two groups that were told to either stick to their usual diet with minor caloric restrictions or to adopt the MIND diet. Both groups received regular dietary counseling, as well as either MIND-compliant foods (for the first group) or money for grocery shopping (for the second). Researchers monitored the participants' weights, diet adherence and blood levels of certain metabolites. 

Ultimately, participants in both groups saw similar cognitive improvements, brain changes and weight loss by the end of the study period.

It's "plausible that practice effects of repeated cognitive testing could account for improvement in both of our trial groups, as has been observed in previous randomized trials," the trial organizers noted in their report. It is also "possible that these interventions do not improve cognitive functioning or that it would take a longer period of adherence for an effect to be observed." 

In short, the study has limitations but hints that, at least in the short term, the MIND diet doesn't offer huge brain benefits over a diet with minimal calorie restrictions. 

Despite decades of Alzheimer's research, scientists have not found a treatment that halts or dramatically slows the disease. Now, scientists are investigating if a completely new approach — so-called Alzheimer's vaccines — could alter the disease's course.

The logic behind this effort? Much of the previous research has placed beta-amyloid plaques, clumps of protein that accumulate in the brains of Alzheimer's patients, front-and-center. But drugs that remove beta-amyloid plaques alone don't seem to have much impact on the disease course. So some researchers have proposed that the plaques are a consequence, rather than a cause of Alzheimer's.

Instead, these researchers say, the disease may result from a badly tuned immune response to an initial bacterial or viral infection, in which the body overproduces inflammation and beta-amyloid while under-activating the cells that normally clear away those proteins away before they cause harm.

In this theory, inflammatory signals reach the brain, stimulating the production of beta-amyloid proteins, which may have antimicrobial properties intended to kill harmful invaders. However, when these proteins confuse healthy brain cells with microbes, they aggregate into plaques that damage the brain. Meanwhile, the cells that would normally mop up beta-amyloid — microglia — are underactive in Alzheimer's.

Related: Brain 'pacemaker' for Alzheimer's shows promise in slowing decline

This idea is bolstered by evidence that people infected with certain viruses, including the herpes virus and potentially SARS-CoV-2, face a heightened risk of later Alzheimer's disease.

Now, researchers are testing vaccines as potential Alzheimer's treatments, in an attempt to retrain the immune system to fight the disease. These vaccines would theoretically work by stimulating the cells that clear beta-amyloid while shutting down the immune cascade responsible for releasing the harmful protein. The shots could both be used to help prevent Alzheimer's and to treat the disease, once it's developed.

One potential Alzheimer's vaccine has existed for a century. 

The tuberculosis vaccine Bacille Calmette-Guérin (BCG) is routinely used in countries where tuberculosis remains a public health risk and is also administered after bladder cancer surgery to summon immune cells to attack lingering cancer cells. In two observational studies comprising thousands of patients, scientists noted that bladder cancer patients inoculated with the BCG vaccine have lower odds of developing Alzheimer's in the next several years. That raised the possibility that the vaccine helps prevent Alzheimer's, at least in the five years after inoculation.

One theory for why BCG might stave off Alzheimer's is that it retrains the immune system. The vaccine induces broad metabolic changes in different groups of immune cells. For example, immune cells called monocytes switched their energy source from glutamine to glucose, which is important for encoding immune memory. This makes immune responses faster while improving pathogen recognition. 

The evidence that BCG is associated with a lower Alzheimer's risk and has long-term immune effects led Charles Greenblatt, a professor of microbiology and molecular genetics at the Hebrew University of Jerusalem and a leader of one of the observational studies, and his colleagues to test BCG as an Alzheimer's vaccine. 

In a proof-of-concept study, the scientists administered BCG to 49 healthy participants around age 65. Nine months later, the researchers found that the vaccination affected the levels of different types of beta-amyloid in participants' blood plasma. The findings suggested that BCG recipients had lower levels of harmful amyloid clumps in their brains, suggestive of a protective effect. 

Now, BCG is being tested in a small clinical trial of 15 adults with mild cognitive impairment and mild-to-moderate Alzheimer's, to see how it affects measurable signs of the conditions. But BCG isn't the only immune-modulating shot being tested in Alzheimer's. 

Related: Shingles vaccine may protect against dementia

Dr. Tanuja Chitnis, a professor of neurology at Harvard Medical School and at Brigham and Women's Hospital, is leading the development of a nasal Alzheimer's vaccine. Called Protollin, the nasal spray was first developed in 2004 as a vaccine additive called an adjuvant, a substance that revs up the immune system. 

Chitnis told Live Science that Protollin is made of bits of bacteria that are recognized by immune cells called macrophages. A 2008 mouse study suggests Protollin doesn't directly train the immune system to attack beta-amyloid but rather broadly activates immune cells so that they eat the proteins. In theory, Protollin could also make the immune cells more responsive to the bacteria and viruses thought to raise the risk of Alzheimer's in the first place.

Current Alzheimer's drugs, like aducanumab and lecanemab, deliver antibodies that specifically stick to and help clear amyloid plaques in the brain. However, the effectiveness of these drugs is highly debated, and they can come with side effects, including brain bleeds, swelling and atrophy. Protollin may avoid the side effects induced by a flood of antibodies, but that said, its safety has yet to be tested in large trials.

Meanwhile, several companies are developing Alzheimer's vaccines that directly target beta-amyloid. Vaxxinity’s UB-311 is the furthest along and its maker is preparing for late-stage clinical trials. Rather than jumpstarting a nonspecific immune response, like Protollin does, UB-311 works by training the body's immune cells to make the antibodies that recognize and clear beta-amyloid. Despite targeting beta-amyloid directly, the manufacturers report that there have been no cases of brain bleeds or swelling in the 43 trial participants — but again, larger trials will be needed to flag potential side effects.  

One side effect to look out for is autoimmunity, James Nowick, a professor of chemistry at the University of California, Irvine who co-authored a review about the potential of Alzheimer's vaccines, told Live Science.

"Once the immune system is activated against an endogenous [body-made] peptide or protein, it is not simple to shut down the activation of the immune system," Nowick said. "A vaccine could thus produce a serious autoimmune response." It isn't as simple as turning inflammation on or off — in Alzheimer's, the microglia aren't active while other processes that release beta-amyloid might be hyperactive. An effective vaccine must work like an orchestra conductor, directing all the components of the brain's immune system in harmony. 

In contrast to the approved antibodies, though, BCG and Protollin have a track-record of safety, as they're already approved for other conditions or as ingredients in other vaccines. But of course, beyond their safety, the effectiveness of these Alzheimer's vaccines also remains to be proven. 

Even if vaccines work no better than existing monoclonal antibodies, though, they could make Alzheimer's treatment more accessible. Aducanumab and lecanemab require repeated infusions and cost patients $26,500 per year, while vaccines might cost only $1,000 per year. 

"In early disease, a few doses may be sufficient to stop the process," Chitnis said. "In more established diseases, ongoing treatment may be required." And if the vaccines leave a lasting mark on immune cells, as seen in some studies of BCG, perhaps that could mean fewer doses or treatments will be required in the long-run. 

People who are vaccinated against shingles in their 70s may reduce their risk of dementia over the next seven years, an analysis suggests.

However, one expert told Live Science that the study is missing a key analysis, the omission of which casts some doubt on the strength of the findings.

Mounting evidence suggests that viral infections may raise the risk of later dementia — conditions that impair one's ability to remember, think and make decisions and affect around 5.8 million people in the U.S. In particular, research has linked shingles infections, caused by the varicella-zoster virus that also causes chickenpox, to an increased dementia risk, although some studies suggest this link may not exist.

After invading the body, varicella-zoster viruses hide within specific nerve cells, where they can lay dormant for decades while being kept in check by the immune system. Later in life, when the immune system works less effectively, the viruses can reactivate and cause shingles, a condition characterized by a painful, blotchy rash that typically appears on one side of the body or face.

Related: A man's rare gene variant may have shielded him from devastating form of early Alzheimer's

In theory, it is the inflammation and other, yet-unknown bodily changes resulting from varicella-zoster reactivation that may increase the risk of dementia, said Ruth Itzhaki, a professor emeritus of molecular neurobiology at the University of Manchester, who was not involved in the new study.

Supporting this theory, previous studies have found lower dementia rates among people who received the shingles vaccine Zostavax compared with unvaccinated people. However, these studies often rest on the assumption any differences in dementia risk are due to vaccination status. In reality, other factors — like a person's likelihood of following diet and exercise recommendations — also play a role and thus muddy the waters of how vaccination, alone, affects disease risk.

To get around this issue, scientists have now analyzed health records collected from people in their late 70s and older, who were living in Wales during the rollout of the Zostavax vaccine in September 2013. People born on or after Sept. 2, 1933 were eligible for the shot, while those born earlier were ineligible. The results of the analysis, which have yet to be peer-reviewed, were posted May 25 to the preprint server medRxiv.

Around 50% of people born in the year following the eligibility cutoff date received the shot during the rollout, the scientists found, and those eligible for the vaccine had lower rates of shingles than those who were ineligible. They then compared dementia rates in people born in the year before the cutoff date with those born within roughly a year after, over a seven-year period after vaccination. In total, this analysis included more than 56,000 people.

People who were eligible for the vaccine were 8.5% less likely to be diagnosed with dementia in the follow-up period, compared with those ineligible. Through further analysis, the scientists estimated that people who were eligible and actually got vaccinated had around a one-fifth lower risk of being diagnosed with dementia, compared with the ineligible group.

However, the scientists did not directly compare dementia rates among people who were eligible and vaccinated with those who were eligible and unvaccinated.

"They have the data to address this question but they give a convoluted, weak rationale to justify why they did not do this," which opens up questions on why they did not present it, Dr. Devangere Devanand, professor of psychiatry and neurology at the Columbia University Medical Center in New York, told Live Science in an email. Still, even with this omission, the findings still add to the idea that shingles may increase the risk of dementia, Devanand said.

"They used a novel method to add further evidence to the idea that viruses may increase the risk of Alzheimer's disease and dementia either through direct damage [to the brain] or inflammation, which has been supported by several other studies," Itzhaki told Live Science.

"I think all these vaccination results [from the current and previous studies] are very exciting," Itzhaki said.

(Note that a newer, more-protective shingles vaccine called Shingrix is now recommended over Zostavax in the U.S., and the study doesn't address Shingrix's effects on dementia risk, the authors noted.)

A man in his 80s gradually started feeling that he was witnessing the same events again and again. This disturbing symptom, somewhat reminiscent of the 1993 movie "Groundhog Day," likely emerged as a rare complication of Alzheimer's disease, according to a new report of the case.

According to the report, published May 16 in the journal BMJ Case Reports, the man once complained to his e-book manufacturer because he thought it kept showing the same material, and he also contacted a technician about his television repeatedly showing the same news. 

When describing his predicament in his own words, he said, "Wherever I go, the same people are on the side of the road, the same cars behind me with the same people in them … the same person gets out of the cars wearing the same clothes, carrying the same bags, saying the same things … nothing is new."

This condition, called deja vecu with recollective confabulation (DVRC), is sometimes seen in neurodegenerative diseases such as Alzheimer's, according to the report. Neurodegenerative diseases are those in which cells of the central nervous system stop working and ultimately die. These conditions worsen over time, and no cures yet exist.

Related: A man's rare gene variant may have shielded him from devastating form of early Alzheimer's 

Deja vecu differs from the more familiar deja vu, the transient and strange feeling that you have experienced the present before. While deja vu describes a fleeting sensation, deja vecu is the persistent perception that new encounters are repetitions of previous experiences. 

Those with deja vecu often lack insight into their condition and develop disabling, delusion-like false beliefs and behaviors to justify their abnormal perception, the case report authors wrote. Collectively, this false perception combined with the production of false evidence to support it is known as recollective confabulation.

DVRC has been described in a handful of other patients with neurodegeneration, including some with Alzheimer's. The exact cause of DVRC remains elusive, but some have suggested that dysfunction of the hippocampus, a part of the brain that helps convert short-term memories into long-term memories, may give rise to a "false sense of recollection," the authors noted.

Deja vecu without recollective confabulation has also been seen in some neurological diseases, including temporal lobe epilepsy and traumatic brain injury, and in psychiatric disorders, such as schizophrenia. In one reported case, it was linked to a person taking 5-hydroxytryptophan, a compound that gets converted into the chemical messenger serotonin in the body. 

A neuropsychological assessment of the man in the recent case revealed memory loss, impulsive behavior and cognitive decline, and he often conflated two separate stories as being just one. Brain scans highlighted unusually low activity in the left temporal lobe, a region of the brain's wrinkled outer layer located behind the left ear, and the frontal lobes, with abnormalities being more pronounced on the right than on the left. 

Doctors also examined the man's cerebrospinal fluid (CSF), the fluid that surrounds and cushions the brain and spinal cord. They found that in the CSF, the level of the protein amyloid beta-42 was reduced, while the tau protein level was borderline elevated. These are signs of Alzheimer's disease. 

The man was treated with a trial of immunotherapy, likely because his doctors had also found antibodies in his CSF, but this treatment was discontinued following a lack of clinical improvement. Four years after the onset of his symptoms, the man scored worse on cognitive tests than he had during his initial assessment. 

"His recollective confabulation symptoms remain pervasive and bothersome," the case report authors wrote. Still, "he continued to live at home and remained independent with self-care."

The largest case series to document DVRC included reports of 13 patients, nine of whom had probable Alzheimer's. Three of the patients had mild cognitive impairment, and one had frontotemporal dementia, the case report authors wrote. They noted that their case report is unique in that it's the first report of DVRC that analyzed brain activity with scans, evaluated the patient's CSF  and included repeated neuropsychological testing.

A newly discovered genetic variant protects against a particularly devastating form of early Alzheimer's disease, raising scientists' hopes of finding treatments that can prevent or slow the progression of this and other forms of the disease. 

The discovery is only the second gene variant reported to protect against autosomal dominant Alzheimer's disease (ADAD), a form of Alzheimer's caused by an inherited genetic mutation. People with ADAD begin to show signs of dementia in their mid-40s and rarely survive past the age of 60, study co-author Dr. Joseph Arboleda-Velasquez, a biomedical researcher at Harvard University, told Live Science. 

The patient at the heart of the new study was a male member of a Colombian family that researchers have been following for a long time because they're known carriers of the genetic mutation that causes ADAD. This man carried that gene, but instead of succumbing to early dementia, he remained healthy into his late sixties and developed only mild Alzheimer's disease by age 72. He died at 73 years old of non-dementia-related causes. 

"It was just really remarkable that he made it that far, despite the odds," Arboleda-Velasquez said. 

Related: New Alzheimer's drug slightly slows cognitive decline. Experts say it's not a silver bullet.

To find out how, Arboleda-Velasquez and his colleagues sequenced the man's genes and came up with a list of genetic variants, or specific versions of genes, that might have been protective. One gene, RELN, popped out as intriguing because the protein it codes for binds to the same cellular receptors as the protein made by a well-known gene called APOE. One variant of the APOE gene raises the risk of Alzheimer's by partially driving the formation of amyloid plaques, clusters of misfolded proteins considered to be a hallmark of Alzheimer's. 

The researchers studied the effects of the RELN gene in cells in lab dishes and in mice and discovered that the variant the man carried actually made the protein that RELN codes for bind more tightly to its receptor. This effect seems to help the RELN protein stabilize the protein tau, which can form tangles in the brain that serve as another tell-tale sign of Alzheimer's.

The patient had reduced tau tangles in many parts of his brain compared to other Alzheimer's patients, but some portions still showed tau pathology. Delving deeper into the gene variant and how it protects against early-onset Alzheimer's is the crucial next step, said Dr. Kenneth Kosik, a neurologist at UC Santa Barbara who studies ADAD but who was not involved in the current research. 

The RELN variant the man carried seemed to have a different effect from the previous protective variant that this same group of researchers reported in another individual in 2019. In that first case, a woman with ADAD did not develop any signs of dementia until her 70s. Although the woman's brain had signs of amyloid plaques, no part of the organ carried high levels of misfolded tau. Instead of a RELN variant, she had an APOE variant to thank for the reduction in malformed tau, the scientists reported.  

Although the two ADAD-resistant individuals had different genetic mechanisms acting in their brains, the ultimate outcome was the same, Arboleda-Velasquez said: Reduced tau pathology and a shocking resilience to Alzheimer's. 

Neurologically, the case of the first woman was easier to unravel than this new case, Kosik told Live Science. APOE is a well-understood gene in the Alzheimer's research community, Kosik said, while RELN's functions are less well-understood.  

"If we understood the mechanism, [how] this gene controls that protein…maybe we can find a drug that would activate that pathway," he said. 

Arboleda-Velasquez and his colleagues have identified other individuals who seem to be healthy despite carrying the mutation for early-onset Alzheimer's, so they intend to continue hunting for genetic variations that confer protection. Though ADAD is only one form of Alzheimer's, it shares the same plaques, tangles, and progression as later-onset disease — only earlier and faster. Thus, researchers are optimistic that a treatment for early-onset Alzheimer's will also protect people who get the disease later in life.

"I think these cases are setting the stage for the next generation of therapies for Alzheimer's," he said.

Alzheimer's disease and related dementias affect an estimated 5.8 million people in the United States, according to the Centers for Disease Control and Prevention (CDC). By 2060, this figure is predicted to rise to 14 million.

Last month, the charity Alzheimer's Research UK launched an online "brain check" tool that suggests people could reduce their risk of dementia by making 12 lifestyle changes, including stopping smoking and cutting back on alcohol. One of the other suggested modifications is challenging the brain, for example by playing crossword puzzles, card games or board games, or by learning a new language.

"The check-in [tool] is based on the latest and strongest available evidence on 'modifiable' risk factors for dementia — the things we may be able to influence," Emma Taylor, an information officer for Alzheimer's Research UK, told Live Science in an email.

But can challenging the brain really help prevent Alzheimer’s disease?

Alzheimer's disease is characterized by specific pathology — amyloid plaques and neurofibrillary tangles, Dr. Deborah Lee, a medical doctor and writer for Dr Fox Online Pharmacy in the U.K, told Live Science in an email. Amyloid plaques are abnormal protein clumps, while neurofibrillary tangles are bundles of nerve fibers. 

Whether and how these tangles and plaques cause Alzheimer's is still unclear, but "it seems highly unlikely that just exercising the brain could prevent or reverse these major changes," Lee said. "Brain training will support residual brain function but is unlikely to provide a therapeutic treatment." 

A study in the New England Journal of Medicine tested whether crossword puzzles or board games can slow disease progression in patients at risk of dementia who show signs of mild cognitive impairment. Among the 107 participants, cognitive scores were improved by crosswords and worsened by games in week 78 of the study. However, the long term implications of these results remain to be seen. In other studies, most specially developed  "brain training" exercises have not been found to prevent or delay the progression of cognitive impairment, said Dr. Bal Athwal, a consultant neurologist at The Wellington Hospital in the U.K.

When it comes to treating Alzheimer’s, a 2017 systematic review in the Journal of Alzheimer’s Disease concluded that, despite some positive findings, sampled studies were not adequate in several areas to say whether or not brain training was an effective treatment for those with Alzheimer’s Disease. 

According to Alzheimer's Research UK, researchers believe challenging the brain helps to build a person's "cognitive reserve" — the brain's ability to adjust to the damage done by diseases such as Alzheimer's and keep working properly. 

A 2022 study in the journal Neurology did find that people with high levels of cognitive reserve by the time they reached the age of 69 were less likely to notice a deterioration in their memory and thinking skills. Having a higher reading ability, challenging work and engaging in social and leisure activities were all linked to slower rates of decline. However, the researchers noted that those who stayed in the study until the end were more likely to be the types of people who were socially and intellectually privileged, therefore having greater cognitive reserves as a result of their experiences and lifestyles, possibly creating biased results. Participants who had more health problems and lower cognitive function were more likely to drop out of the study. 

But that isn't to say that brain training is redundant. Continually practicing cognitive skills — such as paying attention, problem solving and utilizing memory — strengthens neural connections in a similar way to building muscle strength by regular visits to the gym, Lee said. "Brain training can target weaker aspects of brain function and help bring it into line," she said. "It can also improve reaction time." So while research indicates that brain training may help contribute to cognitive reserve, indirectly helping build resilience to Alzheimer’s disease, the results of longer term studies will help us determine just how useful it is. 

“Neuroplasticity” or the brain’s ability to form new connections and neural pathways, may help to prevent cognitive decline. It is also thought that brain training exercises can be particularly beneficial for people who are middle-aged or older, Athwal said, as the activities can help promote and strengthen connections within the brain, helping people to stay mentally active. This was evidenced in a 2011 study in the journal Neuroimage, where researchers concluded that demanding tasks led to improved neural efficiency in older adults.

When it comes to Alzheimer's, however, the research is simply not there to suggest that brain training can either prevent or treat the disease.

Blockbuster action movie star Bruce Willis stepped away from acting in spring 2022 after being diagnosed with aphasia, a neurological disorder that impacts the ability to produce and understand words. Now, Willis' condition has progressed and he's received a new diagnosis of frontotemporal dementia, his family announced Thursday (Feb. 16).

"Unfortunately, challenges with communication are just one symptom of the disease Bruce faces," the statement reads. "While this is painful, it is a relief to finally have a clear diagnosis."

The prevalence of frontotemporal dementia (FTD) is somewhat uncertain, because historically, doctors sometimes misidentified the condition as depression, schizophrenia or Alzheimer's disease, according to University of California, San Francisco (UCSF) Health. Current estimates suggest that FTD is the most common form of dementia diagnosed in people ages 60 and younger, although the condition can affect older people, as well. (Bruce Willis is 67 years old.)

FTD actually describes a group of related conditions, all of which arise from the deterioration of cells in the brain's frontal lobe, located behind the forehead, and temporal lobes, situated on either side of the head near the ears, according to the National Institute on Aging (NIA). These conditions are progressive, meaning they get worse over time, and their exact cause is unknown, although studies have flagged several genetic mutations and abnormal proteins that may be involved. 

Related: 'Universal language network' identified in the brain 

The three types of FTD are behavioral variant frontotemporal dementia (bvFTD), primary progressive aphasia (PPA) and movement-related disorders. The first and most common type, bvFTD, primarily involves cognitive symptoms, including having difficulty planning and remembering the order of steps required to complete a task, acting impulsively and losing interest in activities they used to enjoy. Problems with language or movement may emerge as the condition progresses, according to the NIA.

PPA affects a person's ability to use and understand language; it comes in several forms, which differ in their specific symptoms. As their condition progresses, people with PPA can lose the ability to speak, develop problems with memory and reasoning, and show behavior changes similar to those with bvFTD. 

Finally, there are several movement disorders associated with FTD. These impact the regions of the brain that control movement, as well as those involved in thinking and language, in some cases, according to the NIA.

There is no cure for FTD, nor are there any treatments to slow disease progression, according to Johns Hopkins Medicine. People with FTD may be prescribed medications, such as antidepressants, antipsychotics and sleeping aids, to treat individual symptoms of the disorders. They may also work with speech and language pathologists and physical and occupational therapists to adjust to the changes in their abilities. 

People with FTD can live with the disorders for many years, but as they worsen, they may engage in dangerous behaviors and otherwise lose the ability to care for themselves, according to Stanford Medicine. They also face an increased risk of infections and fall-related injuries. 

"Bruce always believed in using his voice in the world to help others, and to raise awareness about important issues both publicly and privately," the Wills family's statement reads. "We know in our hearts that — if he could today — he would want to respond by bringing global attention and a connectedness with those who are also dealing with this debilitating disease and how it impacts so many individuals and their families."

The U.S. Food and Drug Administration (FDA) recently approved the second-ever drug in a new class of medications designed to treat Alzheimer's disease. 

The drug — lecanemab (brand name Leqembi) — underwent "accelerated approval," which differs from the FDA's standard approval process where drugmakers have to provide direct evidence of a drug's clinical benefit. That said, late-stage trials do suggest that lecanemab slightly slows the rate of cognitive decline when taken in early stages of the disease.

Although sometimes heralded as a "breakthrough" in news coverage, lecanemab has garnered a mixed review from doctors and scientists because of its modest effectiveness and potential side effects, as well as its price tag. Live Science asked experts what they think about lecanemab and what patients should know about the treatment.

"Some people in the field see this as a watershed moment," Dr. Michael Greicius, a professor of neurology at Stanford Medicine, told Live Science in an email. "Others, like myself, do not."

Related: Brain 'pacemaker' for Alzheimer's shows promise in slowing decline 

How does lecanemab work?

Lecanemab, developed by the pharmaceutical companies Eisai and Biogen, is an engineered antibody that's delivered via IV infusion. The antibody latches onto sticky clumps of protein, called amyloid-beta plaques, that accumulate in the brain and in the fluid that surrounds the brain and spinal cord. Once bound, the antibody instructs the immune system to destroy those clumps. Amyloid-beta plaques are a hallmark of Alzheimer's, and for many years, most scientists thought these plaques were the root cause of the disease. 

Proponents of the so-called amyloid hypothesis theorize that a buildup of these plaques sets off a chain reaction that eventually kills brain cells involved in thinking and memory. This idea dominated Alzheimer's research for decades, but it's since been challenged by evidence that amyloid plaques are just one piece of a very complicated puzzle, according to a 2018 review in the journal Frontiers in Neuroscience. 

While the debate surrounding the amyloid hypothesis remains unsettled, the FDA has now approved two drugs that take aim at amyloid-beta plaques. Another anti-amyloid antibody drug, aducanumab (brand name Aduhelm), was approved in 2021. The big question is, do these drugs offer clear benefits to patients?

Is lecanemab effective?

Prior to the approval of aducanumab and lecanemab, drugs called cholinesterase inhibitors and NMDA antagonists were approved to alleviate some of the cognitive and behavioral symptoms of Alzheimer's, according to the National Institute on Aging. These drugs don't target the root cause of the disease, but they can be helpful for managing its effects.

Aducanumab marked the first "disease-modifying" drug approved for Alzheimer's — meaning it directly tackles what scientists believe is a cause of the illness. But its approval stirred controversy because there wasn't strong evidence to suggest it slowed cognitive decline, and the FDA's advisory committee actually recommended that the drug not be approved, according to Nature. 

The FDA approved lecanemab on the basis of a mid-stage trial, which showed the drug cleared amyloid but didn't evaluate whether it slowed cognitive decline. However, the results of a larger, late-stage trial were released in November 2022 and offer evidence that the treatment slows cognitive decline "but debatable evidence that it is clinically impactful," said Dr. Constantine Lyketsos, the Elizabeth Plank Althouse professor for Alzheimer's research at the Johns Hopkins School of Medicine. 

The 18-month trial included about 1,800 people with early Alzheimer’s disease ages 50 to 90, according to a Jan. 5 report in The New England Journal of Medicine (NEJM). Half of the participants received twice-monthly infusions of lecanemab, while the other half received a placebo. Cognitive decline was tracked using the Clinical Dementia Rating-Sum of Boxes (CDR-SB), a 18-point scale where higher numbers indicate worse dementia. After 18 months, the lecanemab group showed a significant decrease in amyloid in the brain, compared with the placebo group. Meanwhile, their CDR-SB scores had increased 1.21 points, while the placebo group's increased 1.66 points, meaning the final scores differed by 0.45 points.

Industry experts have argued that, "for a physician to notice a difference in a patient over 1 years' time the patient needs to decline by at least 1 full point on the CDR-SB," Greicius said. In other words, a difference of 0.45 points might not be noticeable to a doctor, let alone the patient or their caregivers, he told Live Science. 

That said, given the limited length of the clinical trials, we don't yet know if patients who take the drug for longer than 18 months will see cumulative benefits or what the course of disease might look like after patients cease treatment, the NEJM report noted.  

When doctors are speaking with patients about the potential benefits of lecanemab, "it's really down to making sure patients understand how little they can expect," Lyketsos told Live Science. "Until we see a robust effect, I think most people are going to opt out."

What are the potential side effects of lecanemab?

In the late-stage trial, about 26% of the lecanemab group had infusion-related reactions, which included flu-like symptoms, nausea, vomiting and changes in blood pressure, compared with only 7% of the placebo group.

Trial participants also experienced amyloid-related imaging abnormalities (ARIA), structural abnormalities that appear on brain scans and have previously been linked to anti-amyloid antibodies. Of the treated group, 17% had ARIA with bleeding in or on the brain, and nearly 13% had ARIA with brain swelling; that's compared with about 9% and 2% of the placebo group, respectively. Most cases were asymptomatic and resolved on their own, although people sometimes reported symptoms such as headache, visual disturbances, confusion and dizziness.

The FDA mandated that lecanemab's label carry a warning for this side effect and that doctors monitor patients closely for it. "ARIA usually does not have symptoms, although serious and life-threatening events" — like seizures — "rarely may occur," the FDA stated. 

Some evidence suggests that such fatal events may have taken place during the extension phase of trial, in which all trial participants can opt to take the drug, open-label, according to documents obtained by STAT and Science. These records show that three participants died of severe brain bleeding, swelling and seizures after starting to receive the drug during the extension phase; it's unclear whether these participants were previously in the treatment or placebo arm of the study. 

Sources told STAT and Science that they suspect the deaths may be related to ARIA and that lecanemab, in clearing amyloid from the brain, also may have weakened the patients' blood vessels. Eisai attributed two of the deaths to factors unrelated to lecanemab and declined to comment on the third death, Science reported in December 2022. In a written statement to Science, an Eisai spokesperson said "all serious events, including fatalities," are provided to the FDA and other regulatory bodies.

In two of the cases, blood thinners may have worsened patients' bleeding, Science reported. "Personally, I think that someone on blood thinners should not go on these therapies for now," Lyketsos said, citing these cases. 

"I think ARIA can be fairly safely managed by dementia specialists in the tightly controlled setting of a clinical trial," Greicius said. "I am very concerned that if and when lecanemab hits the real world of clinical practice, safety monitoring will, invariably, be less rigorous, which will result in more patient deaths."

Is lecanemab worth the cost?

A year's course of lecanemab will cost an estimated $26,500 per year, although the "actual annualized pricing may vary by patient," according to a statement from Eisai.  

"That's just the cost of the drug," Lyketsos said, not the cost of the actual infusions, regular brain scans needed to check for ARIA, or the initial tests run to confirm the presence of plaques in a patient's brain. "We're talking a whole lot more [than $26,500]," Lyketsos said.

And currently, Medicare covers lecanemab only in the context of approved clinical trials; the same policy applies to aducanumab, according to the Centers for Medicare & Medicaid Services (CMS).

That's because these drugs were granted accelerated approval, which only requires that drugs show a specific, measurable effect on the body, not that they improve a clinical endpoint, such as time to death or disability. Both aducanumab and lecanemab clear amyloid from the brain, but to earn accelerated approval, they didn't have to show they helped people stay sharp longer.

Only if lecanemab earns standard FDA approval would Medicare provide broader coverage for the drug, CMS has stated.

This article is for informational purposes only, and is not meant to offer medical advice.

Alzheimer's disease might be attacking the brain cells responsible for keeping people awake, resulting in daytime napping, according to a new study.

Excessive daytime napping might thus be considered an early symptom of Alzheimer's disease, according to a statement from the University of California, San Francisco (UCSF). 

Some previous studies suggested that such sleepiness in patients with Alzheimer's results directly from poor nighttime sleep due to the disease, while others have suggested that sleep problems might cause the disease to progress. The new study suggests a more direct biological pathway between Alzheimer's disease and daytime sleepiness. 

Related: 6 Big Mysteries of Alzheimer's Disease

In the current study, researchers studied the brains of 13 people who'd had Alzheimer's and died, as well as the brains from seven people who had not had the disease. The researchers specifically examined three parts of the brain that are involved in keeping us awake: the locus coeruleus, the lateral hypothalamic area and the tuberomammillary nucleus. These three parts of the brain work together in a network to keep us awake during the day.

The researchers compared the number of neurons, or brain cells, in these regions in the healthy and diseased brains. They also measured the level of a telltale sign of Alzheimer's: tau proteins. These proteins build up in the brains of patients with Alzheimer's and are thought to slowly destroy brain cells and the connections between them. 

The brains from patients who had Alzheimer's in this study had significant levels of tau tangles in these three brain regions, compared to the brains from people without the disease. What's more, in these three brain regions, people with Alzheimer's had lost up to 75% of their neurons. 

"It's remarkable because it's not just a single brain nucleus that's degenerating, but the whole wakefulness-promoting network," lead author Jun Oh, a research associate at UCSF, said in the statement. "This means that the brain has no way to compensate, because all of these functionally related cell types are being destroyed at the same time."

The researchers also compared the brains from people with Alzheimer's with tissue samples from seven people who had two other forms of dementia caused by the accumulation of tau: progressive supranuclear palsy and corticobasal disease. Results showed that despite the buildup of tau, these brains did not show damage to the neurons that promote wakefulness. 

"It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer's disease," Oh said in the statement. "Understanding why this is the case is something we need to follow up in future research."

Though amyloid proteins, and the plaques that they form, have been the major target in several clinical trials of potential Alzheimer's treatments, increasing evidence suggests that tau proteins play a more direct role in promoting symptoms of the disease, according to the statement. 

The new findings suggest that "we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer's treatments," senior author Dr. Lea Grinberg, an associate professor of neurology and pathology at the UCSF Memory and Aging Center, said in the statement.

The findings were published Monday (Aug. 12) in Alzheimer's & Dementia: The Journal of the Alzheimer's Association.

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• 7 Ways the Mind and Body Change with Age
• 6 Fun Ways to Sharpen Your Memory

Originally published on Live Science.

Alzheimer's disease is a progressive brain disorder and a form of dementia that impacts memory, thinking and behavior. As symptoms grow more severe, the disease can seriously affect a person's ability to perform tasks that would otherwise be deemed routine. There is currently no cure for Alzheimer's, but there are medications available that can temporarily delay symptoms.

"Cognitive decline is the first clinical sign [of Alzheimer's]," said Elizabeth J. Coulson, a professor of neuroscience at the Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research at University of Queensland in Australia. "There are degenerative changes that cause cognitive impairment," she told Live Science. "One of the earliest degenerations occurs in the cholinergic neurons of the basal forebrain, which control attention and higher order cognition, and then the entorhinal cortex and hippocampus, which controls memory."

Around six million Americans are currently living with Alzheimer's, according to the Alzheimer's Association. By 2050, that figure is estimated to be closer to 13 million. Alzheimer's is a disease that prominently impacts older people, with 73% of patients age 75 or older. It is also more common in women, with two-thirds of Alzheimer's patients in the U.S. being women. 

Brain changes and Alzheimer's disease

The first case of Alzheimer's was described in 1906 by Dr. Alois Alzheimer, a German neurologist. Alzheimer identified two of the disease's key physical traits when he examined a woman's brain tissue under a microscope after her death: He found abnormal protein clumps (now known as amyloid plaques) and tangled bundles of nerve fibers (now called neurofibrillary, or tau, tangles).

However, while many people argue that the amyloid plaques are the cause of the disease, others say they are just a biomarker for the disease showing that other physiological processes are wrong and they (the latter) cause the disease, Carson said.

"Recent FDA-approved drugs act to get rid of the beta-amyloid in the brain," she said. "They do this very well, but the cognitive processes are not improved — only a tiny bit less decline than someone without the drug."

Dr. Bradley Hyman, a neurologist and director of the Massachusetts Disease Research Center at Massachusetts General Hospital in Boston, also said that nerve bundles can build up inside nerve cells, and along with increased numbers of plaques, can block communication between nerve cells.

The continued loss of connections between nerve cells damages them to the point that they can no longer function properly in the parts of the brain affecting memory, and the nerve cells eventually die. As more nerve cells die, parts of the brain that control reasoning, language and thinking skills are also affected, and brain tissue begins to shrink.

Researchers also suspect that inflammation (excessive action of immune cells in the brain) plays an important role in the progression of Alzheimer's and is more than a side-effect of the disease, Hyman said.

What causes Alzheimer's disease?

The cause of Alzheimer's disease is unclear, but researchers suspect the disease is triggered by a combination of genetic, lifestyle and environmental factors that affect the brain over time.

"A small percentage of people get Alzheimer's because they have a specific change in their DNA," Coulson said. "These people tend to get early onset rather than late onset. The changes in the DNA are linked to the production of beta amyloid from a precursor protein. We all make some, but these genes mean they make more than is typical."

Early-onset Alzheimer's affects people in the mid 30s to mid 60s, and some forms may be inherited. But early-onset disease represents less than 10% of all people with the disorder, according to the National Institute on Aging. Late-onset Alzheimer's is the more common form of the disease, and its first symptoms may appear after age 65.

"We don't know [the causes]," Coulson said. "But there are risk factors. Brain injury results in more risk, as does having sleep apnea, poor vascular health, being overweight, and having diabetes."

According to the Mayo Clinic, other risk factors include:

• Family History. People whose parents or siblings have Alzheimer's have a somewhat higher risk of the disease.
• Heredity. Genetic mutations, such as inheriting the apolipoprotein-E gene, can contribute to the development of Alzheimer's. (But genetic mutations account for less than 1% of people with Alzheimer's, according to the Mayo Clinic.)
• Down Syndrome. People with Down Syndrome are more at risk for Alzheimer's because they have three copies of chromosome 21, which can lead to developing more amyloid plaques in the brain.
• Mild cognitive impairment (MCI). People with MCI have more memory problems than normal for their age, but symptoms don't interfere with their lives. MCI can increase the risk of developing Alzheimer's.
• Severe head injuries. Head injuries have been linked with an increased risk of Alzheimer's.
• Low education levels. People with less than a high-school education may be at higher risk for Alzheimer's.

What are the symptoms of Alzheimer's disease?

The brain changes associated with Alzheimer's may begin a decade or more before a person begins experiencing symptoms, said Hyman.

The most common early symptom of Alzheimer's is difficulty remembering newly learned information, such as recent conversations, events or people's names, according to the Alzheimer's Association. But not everyone has memory problems initially, and some people may first develop changes in their behavior, language difficulties or vision problems.

According to the Mayo Clinic, symptoms in people with mild-to-moderate forms of Alzheimer's may include:

• Repeating statements and questions over and over.
• Forgetting conversations, appointments or events, and not remembering them later.
• Routinely misplacing possessions, and frequently putting them in illogical places.
• Getting lost in familiar places.
• Forgetting the names of loved ones and everyday objects.
• Trouble finding the right words to identify objects, expressing thoughts or participating in conversations.
• Having difficulty concentrating and thinking, and managing finances.
• Struggling to do once-routine activities, such as cooking and playing a favorite game, and eventually forgetting how to do basic tasks, such as getting dressed or bathing.

Alzheimer's also causes mood and behavior symptoms, including depression, sleeplessness, distrusting others, hallucinations and delusions, loss of inhibitions, mood swings, wandering and pacing and anger or aggression.

People with advanced-stage Alzheimer's experience a severe loss of brain function and become completely dependent on others for their care. According to the National Institutes of Health, symptoms during this stage may include:

• Weight loss
• Skin infections
• Difficulty swallowing
• Seizures
• Groaning, moaning or grunting
• Increased sleeping
• Lack of bladder and bowel control

How is Alzheimer's disease diagnosed?

According to Alzheimer's Disease International, there are over 100 forms of dementia, with Alzheimer's being the most well-known form. It can, therefore, be difficult to accurately diagnose Alzheimer's.

"Typically, Alzheimer's is diagnosed through cognitive testing or neuropsychological tests," Coulson said. During these tests, doctors will assess memory impairment, as well as various other thinking skills, functional abilities and any behavior changes.

"Sometimes, more robust and specific tests are performed by a memory clinic, which can involve several hours of testing," Coulson said. "Sometimes an MRI brain scan is performed to look for which parts of the brain are degenerating, or a CT scan to look for vascular changes."

In the past few years, positron emission tomography (PET) scans of the brain, which can detect whether plaques or tangles are present, have been used to diagnose or monitor the disease, Hyman said. 

However, Coulson said that is not routine, and is only really used for research purposes.

How is Alzheimer's disease treated?

There isn't a cure for Alzheimer's, but there are medications available that treat some of the symptoms of the disease, Hyman said.

Cholinesterase inhibitors are drugs that may help with symptoms such as agitation or depression. These drugs include donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon).

"These drugs manage the function of the nervous system," Coulson said. "They work for a period of time in many people to improve cognition and quality of life, but do not change the course of the disease."

Another medication known as memantine (Namenda) may be used to slow the progression of symptoms in people with moderate to severe Alzheimer's. Some patients may be prescribed antidepressants to control behavioral symptoms.

"In the last 12 months the FDA has approved two drugs targeting amyloid plaques," Coulson said. "They work very well to clear the plaques, but not for improving cognition."

There have been many failed trials of these sorts of drugs, she said. Recently, when given early, there was a statistically significant outcome, but it is unclear whether the benefit is something a person would notice. 

"Some argue that these drugs are given too late in the disease," Coulson said. "They might form part of a treatment in the future, but we shall see. I think a cure is still a way away, but I think better treatments are closer."

Experts agree that in addition to medication, lifestyle factors, such as staying physically, mentally and socially active can all help the brain. A diet rich in fruits, vegetables and whole grains, with moderate amounts of fish, poultry and dairy can also be beneficial.

Additional resources:

• Read what the National Institute of Neurological Disorders and Stroke has to say about Alzheimer's disease.
• Learn more about Alzheimer's in this free book from the National Institute on Aging.
• Find out what's on the horizon in Alzheimer's treatment from the Mayo Clinic.

This article is for informational purposes only and is not meant to offer medical advice.

Researchers are officially defining a new brain disorder that mimics Alzheimer's disease, giving the condition a name and diagnostic criteria, according to a new report.

The disorder will be known as LATE, which stands for limbic-predominant age-related TDP-43 encephalopathy, the report said. LATE has only recently been recognized as a type of dementia, and this is the first time that researchers have come to a consensus about what the disease should be called and how it is distinguished from other brain disorders.

The new report — published today, April 30, in the journal Brain — is the product of a National Institute on Aging (NIA)-sponsored workshop on the condition, which included researchers from more than 20 institutions in six countries. [6 Big Mysteries of Alzheimer's Disease]

Because LATE and Alzheimer's disease have similar symptoms, cases of LATE may have previously been mistaken for cases of Alzheimer's. Recognizing these as two separate disorders will advance research on both conditions, the study authors said.

"The ultimate goal ... is to either prevent or at least be able to treat the causes and the symptoms" of either brain disease, be it Alzheimer's or LATE, said Nina Silverberg, director of the Alzheimer's Disease Centers Program at the NIA and co-chair of the LATE workshop.

"In order to do that, we have to understand what's causing the symptoms," Silverberg told Live Science. "Sorting through who has what [condition] hopefully should help us" with this goal.

There is now an "urgent need" for research on LATE, the report said, as there is much more to learn about the condition, including ways to improve diagnosis and identify risk factors, as well as prevent and treat the disease. Ultimately, the new report is a "starting point for the research to move forward" on this condition, Silverberg said.

LATE vs. Alzheimer's

Dementia isn't a specific disease; rather, the term refers generally to a loss of cognitive functioning, such as declines in memory and thinking ability, that interferes with a person's daily activities. Alzheimer's is the most common type of dementia, but researchers now know that there are many different varieties of the disorder.

Although the symptoms of Alzheimer's and other dementias may be similar, these diseases look different inside the brain. The hallmark of Alzheimer's is the accumulation of plaques, made from proteins called beta-amyloid, and tangles, consisting of a different protein called tau, in the brain.

But recently, researchers have found that not everyone suspected to have Alzheimer's shows these telltale signs in their brains, meaning they actually have a different condition.

In cases of LATE, people have an accumulation of a different protein, called TDP-43, that is misfolded in the brain, according to the report.

What researchers know about LATE

LATE tends to affect the "oldest old" in the population: More than 20% of people over age 85 show signs of the condition, the report said. But more research is needed to better understand how many people have the condition, Silverberg said.

Still, the public health impact of LATE is likely at least as large as that of Alzheimer's, the authors wrote.

LATE affects multiple areas of cognition, including memory, and ultimately impairs everyday activity. It appears that LATE progresses more gradually than Alzheimer's disease, although the two conditions may coincide and cause a more rapid decline than either would alone.

The new report describes three "stages" of LATE, depending on where in the brain TDP-43 is found. (The three areas are the amygdala, hippocampus and middle frontal gyrus.)

Currently, LATE can be diagnosed only after death, during autopsy. But the authors said that they hope the new report spurs research into biomarkers for the disease, so that doctors can diagnose it before death and study it in clinical trials. Finding biomarkers for the disease is also important for the study of Alzheimer's, so researchers can distinguish between the two conditions when a person is alive, the authors said.

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Originally published on Live Science.

Last week, headlines reverberated across the internet with seemingly groundbreaking news: Scientists had found a cause — and with it, a possible cure — of Alzheimer's disease. The culprit, the reports said, was the bacterium that causes gum disease.

But have scientists really solved one of the 21st century's biggest medical mysteries? Experts tell Live Science that caution is needed and that untangling the knotty causes of Alzheimer's disease is far from straightforward.

The most common form of dementia, Alzheimer's disease currently affects more than 5.5 million Americans, according to the National Institutes of Health. In the brains of people with Alzheimer's, abnormal buildup of proteins — called amyloid plaques and tau tangles — slowly destroy brain cells and the connections among them, hindering the individuals' ability to think and remember.

The damage is irreversible, and Alzheimer's does not yet have a cure. Scientists worldwide have been working in high gear to find one, but most drugs that have reached clinical trials have failed. Still, studies are ongoing and researchers remain hopeful. [9 Surprising Risk Factors for Dementia]

But scientists aren't just trying to find a cure; they're also trying to find the cause — or, more likely, the causes — of the disease.

What causes Alzheimer's?

There are two forms of Alzheimer's: early onset and late onset.

Early-onset Alzheimer's typically affects people before age 65, with the symptoms usually showing up in a person's 40s or 50s. This form of the disease is uncommon, affecting just 5 percent of all people with Alzheimer's, according to the Mayo Clinic.

In most cases, scientists know exactly what causes early-onset Alzheimer's: genetic mutations passed down through the family. Mutations in one of three genes — called APP, PSEN1 and PSEN2 — can cause a person to develop the early-onset form of the disease. In fact, a person needs to inherit only one of these genes from one parent for the disease to manifest.

The vast majority of Alzheimer's cases, however, are the late-onset type, which typically affects people over age 65, said Dr. Riddhi Patira, an assistant professor of neurology at the University of Pittsburgh Alzheimer's Disease Research Center.

Late-onset Alzheimer's disease isn't necessarily hereditary; in other words, even if a person's parents both have the late-onset form of the disease, that person is not guaranteed to also get it, Patira said. Among her patients, "this is the most common misconception," she added.

So, what does cause late-onset Alzheimer's?

Scientists don't really know yet. Alzheimer's is likely not simply the result of one cause, but rather a combination of genetic, environmental and lifestyle factors, Patira told Live Science. 

For example, a mutation in a gene called ApoE is thought to increase a person's risk for developing late-onset Alzheimer's, but it does not cause it, Patira said. When people who have taken genetic tests come in with a concern that they have this gene, Patira tells them, "it does increase your risk, but it does not guarantee anything."

ApoE plays a role in how cholesterol moves through the blood, according to the National Institutes of Health. Some evidence suggests that people with high blood pressure and high cholesterol have an increased chance of developing Alzheimer's.

Potential environmental causes include radiation, concussions, trauma and exposure to certain chemicals, Patira said. But really, "any cause [you] can imagine, you will find a study about it in the literature," she said. "Everything is hot in Alzheimer's research because people are really desperate" to find a cure.

But lately, scientists have increasingly turned their attention to microbes.

Microbes take the stage

The study that spurred last week's headlines was published on Jan. 23 in the journal Science Advances. In this study, researchers suggested that Porphyromonas gingivalis, the bacteria that cause a common type of gum disease, may also play a role in Alzheimer's. The researchers found that people with Alzheimer's had these bacteria in their brains.

The majority of the study was conducted in mice, however. In those animals, the team showed that the bacteria were able to travel from the mouth to the brain, where they could inflict damage on brain cells and increase the production of the beta-amyloid proteins that cause the telltale plaques of Alzheimer's. What's more, the researchers found that they could stop this damage in mouse brains by targeting toxic enzymes produced by the bacteria. [7 Ways the Mind and Body Change With Age]

Patira noted that while the new study is "well-done … it was done in mice, and mice's brains are similar to [ours] but not the same." Many studies looking at late-stage Alzheimer's have been conducted on mice — some were successful, some not. But even the successful ones, one after the other, failed when they reached the human stage, Patira said.

In any case, while staying skeptical that the new findings will hold true in humans, she said that the results are "promising."

Keith Fargo, the director of scientific programs and outreach for the Alzheimer's Association, agreed that it's "definitely plausible" that such bacteria could play a role in Alzheimer's. However, he also noted that because the study was conducted in mice, its results shouldn't yet be interpreted as holding true for humans.

The idea that bacterial or viral infections could play a role in the development of Alzheimer's was "a bit out of the mainstream" up until maybe a year ago, Fargo told Live Science. But lately, this idea has gained momentum, as scientists have figured out possible mechanisms for how an infection could lead to the formation of these abnormal protein buildups in the brain.

"There may be some kind of infectious agent that attacks the brain and, as part of the immune system's response to that infectious agent, amyloid plaques may develop," Fargo said. "But it may not necessarily be the amyloid plaque itself that's causing the harm. It could be infectious agents."

The microbes most commonly suspected of playing a role in Alzheimer's are herpesviruses.

This controversial idea has been around for a long time. However, it was bolstered last June, when a study published in the journal Neuron found that the brains of deceased people who'd had Alzheimer's had higher levels of herpesviruses than did the brains of deceased people who had not had Alzheimer's.

But even if a virus plays a role in the development of the disease, it's likely not the only factor.

With herpes, for example, the vast majority of people are infected with a herpesvirus infection before the age of 5, Fargo said. "But only about a third of people over the age of 85 develop Alzheimer's disease," he said. So, if microbes do play a role in Alzheimer's disease, there's also something else going on that makes some people more susceptible to the condition.

Whether infectious agents play a role or even cause Alzheimer's, Fargo wanted to make one thing clear: "There is no reason for anyone to believe that Alzheimer's disease is contagious." 

The golden age

Most scientists in this field are expecting that they will soon learn that there are multiple causes of Alzheimer's, Fargo said. And he said he's hopeful we'll soon understand the disease much more clearly than we do now. "I actually tell people that we are entering a golden age of Alzheimer's research," he said.

Though most drugs that have been developed to targeted Alzheimer's have failed early in clinical trials, there are still trials ongoing and there will be more in the future. "I'm optimistic that at some point in time I will have more things to offer my patients," Patira said.

For now, people can lead a healthy lifestyle to reduce their risk of developing the disease, she said. Indeed, there is increasing evidence that physical, mental and social activities reduce the risk of getting Alzheimer's, according to the Centers for Disease Control and Prevention.

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• 6 Big Mysteries of Alzheimer's Disease
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Originally published on Live Science.

Former U.S. Supreme Court Justice Sandra Day O'Connor — the first woman appointed to the U.S. high court — announced that she had been diagnosed with dementia.

"Some time ago, doctors diagnosed me with the beginning stages of dementia, probably Alzheimer's disease," O'Conner wrote in a public letter dated today (Oct. 23).

Alzheimer's disease is a form of dementia, but how do doctors distinguish between the notorious disease and other forms of dementia? [6 Big Mysteries of Alzheimer's Disease]

Dementia is a general term that encompasses any condition that's linked to the loss of cognitive functioning — such as thinking, remembering and reasoning — and that affects a person's daily functioning, according to the National Institute on Aging.

Everyone loses brain cells or neurons as they age. But a person with dementia loses far more neurons and connections to other neurons that allow important signals to travel through the brain.In its various stages, dementia can affect a person's memory, language, visual perception, problem-solving skills, self-management and ability to pay attention.

"Alzheimer's disease is the most common form of dementia among older people," said Dr. Rawan Tarawneh, a neurologist at The Ohio State University Wexner Medical Center, who is not involved with O'Connor's case.

Typically, the first symptoms of the disease are difficulties with short-term memory, such as having trouble remembering recent conversations, events or people's names, Tarawneh told Live Science. Other early symptoms can include having trouble finding words during conversations or reduced problem-solving abilities, such as in managing finances. Depression and loss of interest in some activities are also common, she said.

As Alzheimer's disease progresses, people can have more difficulty communicating, get lost in places they know well and have poor judgement in social situations, Tarawneh said. People can also experience behavioral changes — such as agitation, irritability, episodes of wandering, hallucinations and delusions — as the disease progresses, she said. "In the most severe cases, a person with Alzheimer's disease may need help with simple activities, such as walking, feeding or dressing themselves," she said.

Buta lot of these symptoms are also common in other types of dementia. So, what makes different dementias, well, different? It comes down to what's happening in the brain.

Alzheimer's or another form of dementia?

A hallmark of Alzheimer's disease that distinguishes it from other forms of dementia is an increase in a type of protein called amyloid in the brain. One of the first biological changes to occur in the brain of a person with Alzheimer's is the buildup of clumps of these proteins, called amyloid plaques, between neurons, which hinders their function. Another characteristic of Alzheimer's disease is a buildup of a different protein, called tau. The buildup of both types of protein leads to neurodegeneration, or brain-cell death.

But unlike amyloid plaques, tau buildup and neurodegeneration aren't unique to Alzheimer's disease; they can also occur in other forms of dementia, said Rebecca Edelmayer, the director of scientific engagement at the Alzheimer's Association. This is why "it can be difficult, sometimes, to determine [what form of dementia a person has] based on cognitive testing and symptoms alone," she said.

Indeed, dementia diagnoses remain a bit shaky. There are "a number of people who get told they have Alzheimer's but they don't actually have it," Edelmayer told Live Science.

To make matters more confusing, many people don't have "pure" Alzheimer's disease or a "pure" other form of dementia, but rather, a mixture of different dementias, Edelmayer said. These can include vascular dementia, which affects the blood vessels in the brain, and Lewy body dementia, which is characterized by the buildup of yet another type of protein in the brain.

"What the scientific field is trying to do now is to create other ways to differentially diagnose individuals' dementia using biomarkers," Edelmayer said. Biomarkers are biological changes in the brain, such as an increase in amyloid plaques, that can determine the presence of a disease. Some of these biomarkers appear in people as early as 10 to 20 years before the person first shows symptoms of dementia, Edelmayer added.

Making the right diagnosis is important, because "all of these different types of dementia are characterized by different biological changes in the brain," Edelmayer said. So, if doctors know exactly what's going on in the brain, they can tailor more-specific treatments to the disease.

Originally published on Live Science.

Imagine you tell your 55-year-old mom you're going to get married and she's too disorganized to help you with the wedding preparations. Or you put your kids on the bus to elementary school and the 57-year-old driver forgets the route.

These are real scenarios, drawn from my clinical work with patients who have young-onset Alzheimer's disease.

This is the other face of dementia — no white hair or wrinkles. And it is relatively common. Approximately 5 percent of Alzheimer's patients are younger than 65.

While the underlying pathology of both young-onset and late-onset Alzheimer's is the same — the abnormal accumulation of proteins called amyloid and tau in the brain — there are significant differences in how the two diseases are experienced.

Patients who are under 65, for example, often have difficulties with language, visual processing and organizing and planning. They have less of the classic memory complaints.

There is also accumulating evidence that young-onset Alzheimer's progresses faster.

Dementia confused with depression

The path to a diagnosis of Alzheimer's or other dementia is often long, meandering and riddled with misdiagnosis.

A correct diagnosis is essential for every patient but especially important for younger people. They are often still working and at risk of losing their jobs. They may have young children. When they tell people that something isn't quite right, they are told they are depressed or must be going through a midlife crisis.

Many times, younger patients will notice changes in their cognition at very early stages. They may notice increased difficulty in organization or planning. They may forget how to do complex tasks or forget appointments. Cognitive impairment is more obvious when completing highly demanding tasks at work or co-ordinating family logistics.

When a young person goes to see their doctor and reports such changes in cognition, the "d" word brought up is usually depression and not dementia.

Until the correct diagnosis is made, there can be many misinterpretations of their changes in thinking — resulting in conflicts with family, friends and colleagues.

Divorce before diagnosis

Initially, a change in personality can be misinterpreted by the partner as indifference, as a midlife crisis or as something else.

There can be a changing of roles within a couple and it is not uncommon for separation or divorce to occur before a diagnosis is even made.

If young children are involved, it can be difficult for them to understand the change in their parent's personality.

Getting services for young-onset Alzheiner's can be especially challenging. There are very few programs that cater to people with dementia under the age of 65.

Support for caregivers and family members of these patients is also lacking. There is a dire need for specialized programs and long-term care facilities that can accommodate those under 65.

'Use it or lose it'

Although we have no cure for any patients with Alzheimer's, there are clinical trials that are targeting the abnormal proteins that build up during the disease.

There is symptomatic medication — such as acetylcholinesterase inhibitors — that can help memory.

We also promote a healthy lifestyle that includes aerobic exercise because evidence shows this can slow neurodegeneration. We want people to remain cognitively active and go on learning to help their brain reserve.

Although patients with young-onset Alzheiner's are impaired in some activities, there are many other activities that they can participate in. "Use it or lose it" is the motto we should live by when it comes to the brain and preserving its function.

Young-onset Alzheimer's is not the only dementia that typically affects the young. Frontotemporal dementia also strikes young people. And although there are differences in presentation in these two illnesses, many of the challenges facing patients are the same.

Ongoing research is required to better understand this disease. While we search for a cure, we need to appreciate the special needs of this population. We need to target research and services to better serve patients and their families.

Carmela Tartaglia, Clinician-Scientist, University Health Network and Associate Professor, University of Toronto

This article is republished from The Conversation under a Creative Commons license. Read the original article. Follow all of the Expert Voices issues and debates — and become part of the discussion — on Facebook, Twitter and Google +. The views expressed are those of the author and do not necessarily reflect the views of the publisher. This version of the article was originally published on Live Science.

Could an aspirin a day keep the Alzheimer's away? If only it were that simple. And yet, new research suggests that there does seem to be some hope that aspirin, one of the most widely used medications in the world, may help to treat some aspects of this devastating brain disease.

Scientists have discovered that aspirin works with certain subcellular machinery in the brain to prevent the buildup of amyloid plaque, sticky blobs of protein around brain cells that are thought to be the primary cause of Alzheimer's disease, according to the new study, which was done in mice.

In the study, mouse experiments revealed that aspirin enhanced the ability of lysosomes, which are sort of like the cells' waste processors and recyclers, to clear amyloid plaque or stop it from forming in the first place. Aspirin should have the same effect on the human form of Alzheimer's, too, said the researchers, who published their findings today (June 2) in The Journal of Neuroscience.

Alzheimer's disease, the most common type of dementia, is a progressive brain disease that affects nearly 6 million Americans and is the sixth-leading cause of death among all U.S. adults, according to the Centers for Disease Control and Prevention. There's no cure, and medications have had very limited success in slowing the progression of the disease. [9 Surprising Risk Factors for Dementia]

Aspirin, also known as acetylsalicylic acid, is an inexpensive drug with a century-long history of being safe in low doses, aside from possible stomach irritation and a small risk of internal bleeding. Many adults take a low-dose aspirin daily as a mild blood thinner to help prevent heart attacks.

In fact, several population-wide studies on aspirin and heart health have found that aspirin may also lower the risk of Alzheimer's disease, albeit modestly. A meta-analysis that Chinese researchers published in March 2018 in the journal Frontiers in Aging Neuroscience reviewed 18 population-wide studies and found that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, was associated with a 20-percent lower risk, on average, of developing Alzheimer's disease.

Aspirin and Alzheimer's

Building on the possible connection between aspirin and Alzheimer's prevention, first observed more than a decade ago, researchers at Rush University Medical Center in Chicago crafted experiments that entailed giving aspirin to mice with a mouse version of Alzheimer's disease and also applying aspirin directly to mouse brain cells growing in the lab.

Both approaches — in vivo and in vitro — appeared to prevent or reverse the biological signs of Alzheimer's disease, said lead study author Kalipada Pahan, a professor of neurological sciences at Rush University.

Aspirin activates a cellular receptor called PPARα, which, in turn, regulates a protein called TFEB, a so-called master regulator of lysosomal activity, Pahan explained. In short, aspirin helps cells clear cellular debris, including proteins that form amyloid plaque. [5 Interesting Facts About Aspirin]

"We expect to see similar results in human brain cells," Pahan told Live Science.

Indeed, other drugs, such as the triglyceride-lowering drug gemfibrozil (sold as Lopid), also target TFEB, Pahan said, but aspirin is safe enough to be available without a prescription and has fewer side effects.

Rajini Rao, a professor of physiology at Johns Hopkins University School of Medicine in Baltimore who was not involved with this research, said the new study "offers an elegant mechanistic explanation for protective effects of aspirin seen at the cellular and model animal level."

However, she noted that it was unclear from the study whether the degree of improvement in amyloid removal would translate into better brain function.

"Results from epidemiological studies on aspirin use and dementia are mixed," Rao told Live Science. "While there have been some indications of protection, other studies have failed to replicate this. Unfortunately, this is the case for virtually every drug used in Alzheimer's trials — over 99 percent have failed in the clinic — which is why Alzheimer's research is especially challenging."

Pahan said that, although aspirin is relatively safe, it does carry some risks when used daily and shouldn't be used casually as an unproven way to treat or prevent Alzheimer's disease. He added that for aspirin to stimulate lysosomal activity, the cellular receptor PPARα needs to be present, and thus any person with Alzheimer's who lacks a sufficient number of PPARα receptors wouldn't benefit from aspirin. That may explain the mixed results of population-wide studies, Pahan said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Alzheimer's disease affects millions of people around the world, but what ultimately causes the debilitating dementia remains unknown. One controversial theory, however, holds that the disease might be the result of a virus, or multiple viruses, infecting the brain.

Now, a new study offers more evidence to bolster this theory. In the study, published today (June 21) in the journal Neuron, researchers found that the brains of deceased people with Alzheimer's disease had higher levels of viruses than the brains of deceased people without Alzheimer's. Specifically, the Alzheimer's brains had up to twice as much of two common strains of herpes viruses than the non-Alzheimer's brains. [6 Big Mysteries of Alzheimer's Disease]

The theory that viruses or other pathogens could play a role in the development of Alzheimer's "is actually a pretty old idea," said lead study author Dr. Benjamin Readhead, an assistant research professor at Arizona State University and adjunct faculty member at the Icahn School of Medicine at Mount Sinai. "Even as early as the 1950s, people have been … positing the potential for some kind of pathogen to be contributing to Alzheimer's disease." Still, these ideas have received much backlash from scientists and medical experts throughout the years.

Readhead and his team didn't set out to look for possible viruses; rather, at first they were trying to find brain networks that existing drugs could be repurposed to target as potential treatments for the disease. "That actually kind of led us down this rabbit hole where we started suspecting that viruses could [explain] some of what we were seeing in these Alzheimer's disease networks," Readhead told Live Science.

In the study — one of the most detailed analyses of Alzheimer's brain tissue done to date — the team analyzed nearly 1,000 postmortem brains of people with and without Alzheimer's disease from multiple brain banks. They sifted through raw RNA and DNA sequences taken from these brain tissues and identified which of these genetic sequences were human and which were not. The non-human genetic sequences were compared to a database that contained genetic data for more 500 different viruses that researchers know can, or are thought to, affect humans.

The herpes virus

Though the idea of a virus or bacterium playing a role in Alzheimer's development has not been historically well-regarded, previous research has looked at the idea. In particular, past research has pointed to connections between Alzheimer's disease and the herpes simplex virus one, or HSV1 (the form of herpes virus that typically causes cold sores).

But in the new study, two different strains of the herpes virus stood out: herpes 6A and herpes 7.

And while it may sound startling to learn that there are strains of herpes in the brain, "the thing to say about these viruses is that they're very, very common," Readhead said. (Nearly everyone carries these herpes strains in their bodies because they are infected with them in infancy. However, the strains don't typically cause problems other than rashes in young children.) In fact, the researchers detected the presence of these viruses in about 40 to 50 percent of the brain tissues examined in the study. But the Alzheimer's brain samples had many more copies of these viruses than those without, he said.

Because viruses were found in both Alzheimer's brain tissue and non-Alzheimer's brain tissue, the researchers can't "simply say that infection with these viruses causes Alzheimer's disease," Readhead said. "There's obviously some other important mechanisms that change why some people would have a different response to the presence of a virus."

Still, the viruses may play a role: They could be part of the cause, or they could also just serve to accelerate the disease, Readhead said. Or maybe they don't play a role at all, and just happen to be along for the ride, he added.

To better elucidate the role, if any, of the viruses, the researchers looked to see if any of the viruses were affecting proteins and genes known to be implicated in Alzheimer's.

"There were actually quite a few different viruses that we saw [connected] in some interesting ways to different aspects of Alzheimer's," Readhead said. For example, the herpes 6A virus was found to interact with a large number of genes linked to Alzheimer's disease risk, as well as genes related to amyloid plaques, which are protein clumps that form in the brains of people with the disease.

Still, more research is needed. "One of the real outstanding questions to this is trying to determine the extent [to which] what we're seeing could be a causal contributor to the disease," Readhead said. 

But which herpes virus is it?

Hugo Lövheim, a senior lecturer in the Department of Community Medicine and Rehabilitation at Umeå University in Sweden who was not part of the study, praised the new research.

"The authors have performed a really impressive in-depth analysis of postmortem Alzheimer’s disease brain tissue samples using modern bioinformatics techniques," Lövheim told Live Science. "This is in line with the now rapidly increasing evidence of viral infections as key drivers in the development of Alzheimer’s disease pathology." [9 Surprising Risk Factors for Dementia]

However, Lövheim noted that he still believes HSV1 "is a more likely cause of the disease" at its onset. The new study, along with some earlier research, he said, indicates that the herpes 6A virus may play a role at least in late Alzheimer’s disease. Therefore, future Alzheimer's drug research could aim to target both strains of the virus, he said.

Ruth Itzhaki, a professor emeritus of neuroscience and experimental psychology at the University of  Manchester in England was also not a part of the new study, but was the first researcher to point to the possible role of HSV1 in Alzheimer's, back in 1991.

Itzhaki told Live Science in an email that she still thinks HSV1 has a stronger link to Alzheimer's, but that the viruses could be working together.

"It’s good that the viral concept is now being taken seriously, because during almost all of 28 years, I and subsequently others have suffered venomous hostility, derision or neglect from influential people in the field," she said.

Originally published on Live Science.

For women, physical fitness in midlife may do more than give the heart a boost; it may also benefit the brain, a new study from Sweden suggests.

Researchers found that middle-age women in Sweden with a high degree of cardiovascular fitness were nearly 90 percent less likely to develop dementia later in life than those who had a moderate fitness level. The findings were published today (March 14) in the journal Neurology.

What's more, if women in the fittest category did develop dementia, these problems — such as trouble with memory and thinking — tended to emerge, on average, 11 years later than among women in the moderate fitness group. So, the onset of dementia may have occurred at age 90 in a woman who was considered extremely fit woman at midlife, compared with age 79 in a moderately fit woman. [9 Surprising Risk Factors for Dementia]

The findings suggest that high cardiovascular fitness is associated with a decreased risk of dementia, said lead author Helena Horder, a researcher at the Centre for Aging and Health at the University of Gothenburg in Sweden. In other words, good heart health is linked with good brain health, she said.

In the study, researchers looked at data from 191 women in Sweden ages 38 to 60. At the start of the study, in 1968, all of the middle-age women were given an exercise test on a stationary bike in which they cycled until they felt exhausted.

After tracking the women for 44 years, the researchers found that those fitness test scores helped predict whether the women would be diagnosed with dementia later in life. The analysis showed that 32 percent of the women with a low fitness score developed dementia during the study period, compared with 25 percent of those women with a medium fitness score and 5 percent of the highly fit women.

But the highest dementia rates were seen in women who started the exercise test but could not complete it: 45 percent of these women went on to develop dementia. The researchers suspect that some underlying cardiovascular processes — such as high blood pressure— in middle age might have made these women more vulnerable to dementia decades later.

Good for the heart and brain

Although the findings found an association between cardiovascular fitness and the risk of dementia, this study did not establish a cause-and-effect relationship between the two, the researchers said. It's not clear why a woman's fitness level at midlife might reduce her likelihood of dementia

It could be that improved fitness has a protective effect by reducing various cardiac risk factors, such as lowering blood pressure, creating a healthier body weight and producing a better lipid profile, Horder told Live Science. Emerging evidence also suggests that cardiovascular fitness may directly affect structures in the brain, by increasing blood flow to them, she noted.

Previous studies have established a connection between fitness and dementia, but some of them relied on people's self-reported levels of physical activity and did not involve exercise testing. In studies that have shown a link between physical activity and dementia, it's not clear whether the mechanism that may be responsible for the brain benefits is an enriched social environment and cognitive stimulation or the actual improvement in fitness level, Horder said.

One of the strengths of the new study is its long follow-up period from middle age to the golden years. But the researchers acknowledged that the study had limitations. For example, because the research looked at only Swedish women, the results may not be generalizable to other populations. In addition, the study was relatively small, with fewer than 200 women, and it evaluated cardiovascular fitness at only one point in time using an exercise test that may be done differently now than it was in 1968.

However, because there is not yet a cure for dementia, efforts, in general, have also focused on ways to modify people's behaviors to potentially delay or prevent the condition's onset, Horder said. Based on these and other findings, improved cardiovascular fitness through physical activity may be one of these potential approaches, she noted.

An editorial accompanying the new study suggested that additional research is needed to determine whether the link between fitness and dementia is due solely to the influence of heart health on brain health, or whether physical activity influences the brain independently of the activity's cardiovascular effects. But the editorial ultimately concluded that "What is good for the heart really does seem to be good for the brain also."

Originally published on Live Science.

Risk Factors

The statistics surrounding dementia are staggering: Worldwide, an estimated 47 million people live with this disease, and nearly a trillion dollars is spent annually to care for these individuals, according to Alzheimer's Disease International. In the U.S. specifically, an estimated 4.5 million people have dementia, and that number is expected to grow to about 14 million by 2050.

Dementia refers to a group of symptoms — such as memory loss and problems with communication — that result from changes in the brain. Many diseases and conditions can cause dementia, including Alzheimer's disease.

But traditionally, dementia and, more specifically, Alzheimer's have not been thought of as preventable diseases. Given the staggering statistics, however, more money has been spent to identify causes of dementia and ways to possibly help prevent the disease.

And although some risk factors, such as genes, cannot be modified, other small lifestyle changes could help you feed your brain and keep it sharp for years down the line.

Here are nine recent studies that are changing the way we think about how to prevent dementia.

Snoring

It turns out that snoring can be harmful to more than your marriage: A May 2017 study published in the journal Sleep found that a sleep condition called obstructive sleep apnea (OSA) was linked to a greater Alzheimer's risk.

OSA is a condition in which breathing starts and stops during sleep. These small interruptions can decrease oxygen supply to vital organs and have already been linked to high blood pressure and heart disease. The new study, however, shows that these episodes may also be tied to poorer cognitive performance and an increased risk of dementia. This risk has also been seen with molecular studies that show changes in the spinal fluid of patients with OSA, that suggest early changes in substances tied to Alzheimer's, compared with people who didn't have OSA.

But there's good news: The findings suggest that by treating OSA, you may be able to lower your risk.

Drinking diet soda

While it's certainly not surprising that soda can be hazardous to your health, recent research published in April 2017 in the journal Stroke provided strong evidence that diet soda may increase your risk of dementia, perhaps even more than regular soda alone.

The study looked at approximately 3,000 patients over age 45 who self-reported their beverage intake using a questionnaire. After adjusting for factors such as age, sex, physical activity, smoking and education, those who had a more recent and higher intake of artificially sweetened drinks were found to be three times more likely to develop dementia than those who drank less diet soda.

Interestingly, sugar-sweetened beverages, including fruit juice and nondiet sodas, were not associated with dementia risk.

Why would this be the case? Some of it probably is "self-selecting," meaning that people who are already unhealthy might be more likely to choose a diet drink. But the researchers noted that there is growing evidence for a direct effect from the artificial sweeteners themselves. Still, more research is needed to confirm the findings and establish a cause-and-effect relationship.

Low education and hearing loss

The way you live your life appears have a significant impact on dementia risk: A comprehensive report, published in July 2017 in the journal The Lancet, concluded that one-third of dementia cases could, theoretically, be prevented by lifestyle modification.

Surprisingly, some of the risk factors — such as low education levels, hearing loss in middle age and social isolation — were associated with risks approximately equal to those of smoking, obesity and high blood pressure. The researchers concluded that certain interventions like educating everyone beyond the age of 15 and treating everyone for hearing loss in middle age would reduce the number of dementia cases by 8 and 9 percent, respectively.

Increasing education, for example, may reduce dementia risk by increasing the mind's resilience to brain damage caused by aging, the researchers said. And by treating hearing loss, you can also cut into other risk factors for dementia, including depression and isolation.

Calcium supplements

Could you be building a strong body at the price of a strong mind?

Though calcium can help build strong bones, over the past several years, calcium supplements have become controversial.

An August 2016 study in the journal Neurology found that for women who already had signs of cerebrovascular disease (think heart disease of the brain), those who took calcium supplements were twice as likely to develop dementia than those who did not take them. In addition, those who had already had a stroke and took calcium supplements were seven times more likely to develop dementia than those who didn't take the pills.

The study only found an association between calcium supplements and dementia — it did not show cause and effect — and more research is needed to confirm the findings. However, the scientists said the link between the two may be explained because calcium pills could alter blood vessels and blood flow to the brain, which, in turn, could cause changes that lead to dementia.

Dizziness

At some point, you may have stood up too quickly and gotten light-headed. For some people, however, this feeling happens more frequently — a condition called orthostatic hypotension — and is a sign your blood pressure may drop more than it is supposed to when you go from lying down to standing up. This could mean your brain might not get the same healthy supply of blood when you stand up.

According to an October 2016 study published in the journal PLOS Medicine, older adults who experienced these drops in blood pressure had a 15-percent increase in their risk of developing dementia compared with those who didn't experience these blood pressure changes. And those who had a drop in blood pressure and no increase in their heart rate to help getting the blood flowing again had an even higher risk, 39 percent.

Thankfully, treatment for this condition may be as simple as making some lifestyle changes, according to the Mayo Clinic, including getting out of bed slowly, drinking enough water and doing exercises to help increase blood flow to the brain, such as crossing and tightening your leg muscles while standing.

ADHD

Though attention deficit hyperactivity disorder (ADHD) is primarily thought of as a disorder in children, around 4 percent of adults in the U.S. also have the condition, according to the National Institutes of Health.

Recent research published in June 2017 in the Journal of Attention Disorders suggests that people diagnosed with ADHD as adults are more likely to be diagnosed with dementia and mild cognitive impairment later in life, compared with adults who don't have ADHD. In that study, researchers found that adults with ADHD had a 3.4 times higher risk of developing dementia over a 10-year period compared with adults without ADHD.

The researchers said that the mechanism linking the two conditions "remains unclear." For example, there are questions about how much symptoms overlap between the conditions, and previous research has noted that it is hard to say for certain if ADHD leads to dementia through an unknown mechanism, early dementia symptoms are being misdiagnosed as ADHD or the two disorders exist along a spectrum.

An unhealthy heart

The connection between the heart and the mind is well established, and recent research suggests that keeping your heart healthy may give your brain a boost.

In this case, the connection likely lies in the health of your blood vessels. Things that can damage vessels — including high blood pressure, diabetes and, possibly, smoking — not only increase your risk of heart disease but can also raise your risk of dementia, according to a February 2017 study.

That study, presented at the American Stroke Association's International Stroke Conference in Houston, followed about 50,000 adults for 25 years. The researchers observed that the people who had high blood pressure or diabetes or were smokers had an increased risk of dementia, compared with those without these risk factors. The risk of dementia was increased by up to 77 percent for people with diabetes and 41 percent for smokers.

The researchers noted that although the study doesn't prove that protecting your heart will lower your dementia risk, eating a healthy diet and controlling blood pressure likely help to protect your brain from the small-blood-vessel problems and plaque buildup that are known to contribute to dementia.

Decreased REM sleep

Do sweet dreams protect your brain?

An August 2017 study published in the journal Neurology found that older adults who spent less time in REM, or rapid-eye movement, sleep were more likely to develop dementia over a 12-year period than those who got more REM sleep.

REM sleep is the part of the sleep cycle that's defined by high levels of brain activity and, most notably, when most dreaming takes place.

In the study, the researchers found that adults who spent an average of 17 percent of their sleep in REM were more likely to develop dementia, compared with adults who spent 20 percent of their snoozing in REM sleep.

Though the study showed an association between decreased REM sleep and dementia — rather than proving cause and effect — the researchers noted several possible explanations for the link. It's possible, for example, that the high levels of brain activity during REM sleep help promote and protect certain neuropathways that are vulnerable to damage with aging. It may also be that decreased REM sleep is a byproduct of other known risk factors for dementia, such as anxiety and stress.

Head injuries

There's mounting evidence showing that repetitive blows to the head can lead to serious brain disease, namely chronic traumatic encephalopathy, or CTE. What's less clear, however, is how head injuries (both repetitive and nonrepetitive) are linked to other forms of dementia, such as Alzheimer’s.

But a large meta-analysis published in January 2017 in the journal PLOS ONE showed that head injuries are associated with an increased risk of dementia and, in particular, Alzheimer’s disease.

The meta-analysis looked at 32 studies that represented more than 2 million people in total, and included more than 13,000 cases of dementia and 8,000 cases of Alzheimer's disease. The analysis found that those who had a history of head or traumatic brain injury (such as a concussion) had a 60-percent increased risk of dementia, and a 50-percent increased risk of Alzheimer's disease, compared with those who hadn't had head or brain injuries.

Interestingly, this risk was not increased if a person lost consciousness as a result of the injury.

Other research looking at proteins in the brain, and particularly those that lead to plaque deposits seen with Alzheimer's, found that these proteins can be seen as early as 2 hours after a severe head injury.

Implanting a pacemaker-like device in the brains of people with Alzheimer's disease could help slow the decline in decision-making and problem-solving skills that's typically seen in these patients, a new study suggests.

The small study involved three patients with Alzheimer's disease who had a deep-brain-stimulation (DBS) device implanted in their frontal lobe — a part of the brain tied to "executive functions," which include planning, problem-solving, attention and judgment. The implant, sometimes called a "brain pacemaker," consists of thin electrical wires connected to a battery pack that sends electrical impulses into the brain.

The study — published online today (Jan. 30) in the Journal of Alzheimer's Disease — found that after about two years, patients with the DBS implant showed less of a decline in executive functions, compared with a group of similar patients with Alzheimer's who didn't receive implants.

The study is the first to attempt to use deep-brain stimulation to target symptoms related to executive function. Previous studies have used DBS in Alzheimer's patients to target parts of the brain thought to be involved in memory. [6 Big Mysteries of Alzheimer's Disease]

"We have many memory aides, tools and pharmaceutical treatments to help Alzheimer's patients with memory, but we don't have anything to help with improving their judgments, making good decisions, or increasing their ability to selectively focus attention on the task at hand and avoid distractions," co-author of the study Dr. Douglas Scharre, the director of the Division of Cognitive Neurology at Ohio State's Wexner Medical Center's Neurological Institute, said in a statement. "These skills are necessary in performing daily tasks such as making the bed, choosing what to eat and having meaningful socializing with friends and family," Scharre said.

Because the study was small, it will need to be repeated in a much larger group of Alzheimer's patients, said Dr. Michael Schulder, vice chairman of neurosurgery at North Shore University Hospital in Manhasset, New York, who was not involved with the study.

Deep-brain stimulation has been used to treat a number of neurological conditions, including Parkinson's disease, tremors, depression and obsessive-compulsive disorder. It's not clear exactly how DBS works to improve patients' conditions, Schulder said, but it may help block signals that interfere with normal brain function, or it may help brain cells work better. The treatment could also work differently in different parts of the brain, he added.

In the new study, DBS implants were placed in a part of the frontal lobe called the ventral striatum. Participants periodically completed a test intended to measure aspects of cognitive function that are affected by Alzheimer's disease, including executive functioning and the ability to carry out basic daily activities. The participants with the implants were compared to a group of about 100 people with Alzheimer's disease who were around the same age and had similar levels of cognitive impairment, but did not receive DBS.

The researchers found that two of the three patients who received the implants showed significantly less decline in their test scores, compared with the participants who didn't receive the implants. One of the DBS participants, 85-year-old LaVonne Moore of Delaware, Ohio, even showed some improvement in her daily activities. For example, when Moore started the study in 2013, she wasn't preparing her own meals. But after two years with the implant, she could  cook a simple meal, the researchers said.

In the future, the researchers want to explore using nonsurgical methods to stimulate the frontal lobe in Alzheimer's patients, which would be a less invasive treatment than the surgery required for DBS.

Schulder said that DBS treatments "would only be one small part of the puzzle" in treating Alzheimer's. Ultimately, tackling Alzheimer's will require multiple components, including preventive measures and medications, as well as approaches such as surgically implanted devices that stimulate multiple parts of the brain, he said.

Original article on Live Science.

Injecting the blood plasma of healthy young people into people with Alzheimer's disease appears to be safe, and the practice may even lead to small improvements in daily functioning in Alzheimer's patients, a new small trial suggests.

But not all experts are lining up behind this technique, and instead argue that the science simply isn't there yet to support it. 

It sounds a little (OK, a lot) sci-fi: infusing old people with young blood to reverse the scars of aging and disease. Indeed, the concept is more speculative than most science that makes it to the human-testing phase. No one knows why young blood might help improve a degenerative disease like Alzheimer's, and the vast majority of the research so far has been done in rodents. If it works — and that is far from certain — it's a total mystery as to why.

"It's outside of the box," said Dr. Sharon Sha, a neurologist at Stanford University School of Medicine who led the new trial on the safety of the treatment. The research team is making no grand claims about a cure for dementia, Sha told Live Science, but rather wants to push the research forward in the knowledge that it's safe for humans. [6 Big Mysteries of Alzheimer's Disease]

Blood swap

The results of the new trial, which the researchers presented Nov. 4 at the Clinical Trials on Alzheimer's Disease 10th annual meeting in Boston, focused on people with mild or moderate Alzheimer's disease. In the first portion of the trial, nine patients were given either an infusion of blood plasma (the clear portion of blood that contains clotting factors and immune cells, but no red blood cells) or a placebo weekly for four straight weeks. They then went six weeks without treatment and returned for a final four weeks of getting either the plasma or the placebo — whatever they hadn't received the first time. Neither the researchers nor the patients knew which treatment they were receiving at any given time. The patients took cognitive assessments before and after each portion of the trial. They also took assessments of their daily living abilities, such as the ability to pay bills or balance a checkbook, before and after the treatments.

In the second half of the trial, another nine patients took baseline cognitive and daily functioning assessments, got four weeks of weekly plasma infusions and then took another round of assessments.

The main point of the study, Sha said, was to ensure that the plasma treatments were safe. Plasma is already used for conditions in which the body has lost a lot of blood or needs help with clotting, but it can sometimes trigger itching or immune reactions, Sha said. Another concern was whether the plasma transfusions would raise the patients' blood pressure.

There was no evidence of negative side effects from the treatment, the researchers found. And they found tantalizing hints that it might also be useful: Although the plasma treatments didn't alter the patients' scores on cognitive testing, the patients did show small improvements in their ability to function on a daily basis.

Timing concerns

The study wasn't really designed to look for detailed outcomes, Sha said, so it's not clear why improvements showed up in daily functioning but not thinking abilities. It's possible that the cognitive measurements the team used were too broad, or that the four-week time frame of the study was too short, she said. Or perhaps the treatments simply don't do much for cognitive abilities, or even functional abilities.

"The fact that we found some improvement in functional abilities is exciting and promising, but it doesn't mean that it proves improved functional abilities," Sha said. For that, the researchers need a larger human trial spanning a longer time frame, she said.

But not all researchers think that transfusions of young blood will lead to meaningful medical treatments. The new study proves neither benefit nor safety, said Irina Conboy, a professor of bioengineering at the University of California, Berkeley.

For Conboy, who was not involved in the research, larger human trials are premature. The study conducted by Sha and her colleagues was too short-term to determine either benefit or harm from the transfusions, she said. Moreover, the decision to do transfusions for only four weeks seems arbitrary, Conboy told Live Science, and the patients weren't tracked long enough to see long-term side effects, like the development of autoimmune problems, which can take years. [11 Surprising Facts About the Immune System]

"How do you know that, after five weeks, you would not see improvement or something really bad, like side effects?" Conboy said. "Why did you do four weeks and then you stopped?"

Mystery mechanism

The idea of transfusing new blood into old bodies dates back to the 1950s, when researchers would surgically attach two animals (usually rats) so that they shared a blood flow — a process called parabiosis. This method was often used to study metabolism. More recently, scientists have become interested in using parabiosis to understand and attempt to slow aging. In 2012, for example, University of Cambridge-led research found that linking the blood flow of old mice to young mice led to the formation of new myelin in the central nervous systems of the old mice. Myelin is the fatty sheeting that surrounds nerve cells and enables them to conduct electricity rapidly. Since myelination declines with age and in chronic diseases like multiple sclerosis, the researchers hoped that they could isolate something in young blood that drives remyelination in old brains.

The new Alzheimer's trials came out of research done by Tony Wyss-Coray, a Stanford neuroscientist and the founder of the startup Alkahest, which aims to find the factors in blood that promote tissue regeneration. Alkahest was responsible for the current human trial, in collaboration with Sha's Stanford lab. Earlier this year in the journal Nature, Wyss-Coray and his colleagues reported that giving plasma from human umbilical-cord blood to old mice improved the function of the hippocampus, a brain region involved in memory and spatial reasoning, in the mice. The study also found an increase in a blood factor called tissue inhibitor of metalloproteinases 2 (TIMP2) in the brains of the transfused mice, suggesting a possible culprit for the improvement.

TIMP2 isn't the only possibility, though. Another study by Wyss-Coray's team, this one published in the journal Nature Medicine in 2014, found similar improvements in cognitive function in old mice given blood from young mice that, in part, seemed due to the activation of a protein called Creb, or cyclic AMP response element binding protein. It may be a combination of factors, not just one do-it-all protein, that makes the difference, Sha said. [Extending Life: 7 Ways to Live Past 100]

But Conboy noted that these animal studies used older, but not elderly, mice. Those studies were the equivalent of testing the transfusions on healthy 60-year-old humans without dementia, she said. There are animal models of Alzheimer's disease, including genetically modified mice, but tests using those models haven't been done, Conboy said. Nor have the results from Wyss-Coray's team been replicated by outside research groups.

"Typically, before we start any procedure in clinical trials, we do work with animals that model that particular disease, which was not done in this case," Conboy said. Replications of the mouse work should be the next step, she said, not further human testing. Her research, she added, has found that infusions of young blood are not typically enough to alter the physiology of old bodies. In older cells, multiple proteins and molecules are overproduced, and those need to be regulated downward to see therapeutic benefit, Conboy said. Young blood alone can't overpower these effects of age.

Wyss-Coray and his team, on the other hand, think there is some sort of anti-aging power in the blood of the young. Ultimately, the goal is to find these factors and re-create them as a medication, Sha said. "I think we wouldn't want to rely on the youthful population" to donate blood to the elderly, she said.

"There's hope, and people are working on it," Sha said. "It's not the answer yet."

Original article on Live Science. 

Decreased blood flow from the hearts of older adults may lead to decreased blood flow in areas of the brain responsible for memory — a finding that may reveal a possible link between heart problems and Alzheimer's disease, a new study finds.

The researchers found that people in the study whose hearts pump less blood than they should tend to experience significant problems with blood flow to the left and right temporal lobes of their brains ¾ areas that are involved in memory, and that tend to shrink in cases of Alzheimer's disease.

"We've known for some time that individuals with Alzheimer's have changes in blood flow in the brain," said co-study author Angela Jefferson, the director of the Vanderbilt Memory & Alzheimer's Center at Vanderbilt University Medical Center. [Extending Life: 7 Ways to Live Past 100]

But this is the first time a direct link has been drawn between those blood-flow issues and heart health, Jefferson told Live Science.

The findings, which were published today (Nov. 8) in the journal Neurology, come from an ongoing, far-reaching project at Vanderbilt to collect data on the relationship between lifestyle and physical health issues, and problems in aging brains. In the current study, more than 300 people with an average age of 73 who had no severe heart or brain diseases sat through echocardiograms to measure the strength of their hearts. They also underwent MRIs to measure blood flow in their brains.

The researchers found that for every one-unit decrease in cardiac index — a measure doctors use to pinpoint heart strength ¾ the left temporal lobe experienced, on average, the same decrease in blood flow that's typically associated with 15 years of aging, and the right temporal lobe went through a blood-flow decrease typically associated with 20 years of aging.

The patients' "cerebrovascular reactivity," or the brains' ability to increase blood flow when it needs to, also significantly suffered, the researchers found.

Jefferson cautioned, however, that it's important not to overread the results of the study. For example, the data is "cross-sectional," which means that each patient's measurements were taken from just a single moment in time. Without looking at how those numbers change in relationship to one another over time, it's impossible to be sure that heart problems cause these brain problems, Jefferson said.

It's entirely possible that the reverse may be true: that the blood-flow problems researchers observed in the brain lead to heart problems, or that both result from some unknown third factor, she said. And even if heart problems play a role in cognitive decline, they are likely not the only culprit.

Still, the results here are an "exciting first step" for researchers interested in all of those questions, Jefferson said.

Originally published on Live Science.

The levels of magnesium in your blood may be linked to your risk of developing dementia later in life, a new study from the Netherlands finds.

Compared with people in the study who had high or low levels of the mineral in their blood, those with levels in the middle range were less likely to develop dementia, according to the study, which was published online today (Sept. 20) in the journal Neurology.

Lead study author Dr. Brenda Kieboom, an epidemiologist at Erasmus University Medical Center in the Netherlands, said in a statement that "the results are intriguing." [6 Big Mysteries of Alzheimer's Disease]

The study did not prove that high or low levels of magnesium in the blood cause dementia, Kieboom said; rather, it showed only an association between blood magnesium levels and dementia risk. The findings "need to be confirmed with additional studies," but if they hold up, it's possible that blood tests to measure magnesium levels could one day be used to help determine who is at risk of developing dementia, Kieboom said.

Previous research suggested two possible ways that magnesium could play a role in the development of dementia, according to the study. Magnesium regulates a receptor in the brain that plays an important role in memory and learning. In addition, low levels of magnesium have been linked to inflammation, which could increase dementia risk.

The study involved nearly 10,000 older adults living in the city of Rotterdam, in the Netherlands. At the beginning of the study, when the average age of the participants was 65, the people were screened for dementia, and their blood magnesium levels were measured. The participants were then followed for an average of eight years.

The researchers divided the people into five groups based on their blood levels of magnesium, and found that the people in the highest and the lowest blood magnesium groups were each about 30 percent more likely to develop dementia during the study period than those in the middle group.

Nearly all of the people in the study had magnesium levels that fell within what doctors consider a normal range, according to the study. Normal blood magnesium levels range from 0.85 millimoles per liter (mmol/L) to 1.10 mmol/L, according to the National Library of Medicine. The lowest group in the study had magnesium levels of 0.79 mmol/L or lower, and those in the highest group had levels of 0.9 mmol/L or above.

The researchers noted that the study had limitations. For example, magnesium levels were measured only once, at the beginning of the study, and could have changed over the study period. In addition, it's possible that blood magnesium levels don't fully represent the total amount of the mineral in a person's body, the researchers said.

Earlier studies have linked blood magnesium levels to other neurological conditions, including migraines and epilepsy.

Originally published on Live Science.

An artificial-intelligence-driven algorithm can recognize the early signs of dementia in brain scans, and may accurately predict who will develop Alzheimer’s disease up to two years in advance, a new study finds.

The algorithm — which accurately predicted probable Alzheimer's disease 84 percent of the time — could be particularly useful in selecting patients for clinical trials for drugs intended to delay disease onset, said lead study author Sulantha Sanjeewa, a computer scientist at McGill University in Canada.

“If you can tell from a group of of individuals who is the one that will develop the disease, one can better test new medications that could be capable of preventing the disease,” said co-lead study author Dr. Pedro Rosa-Neto, an associate professor of neurology, neurosurgery and psychiatry, also at McGill University. [6 Big Mysteries of Alzheimer's Disease]

The technology is still in its early stages, but the findings suggest that AI analysis of brain scans could offer better results than relying on humans alone, Rosa-Neto told Live Science.

The findings are detailed in a new study, which was published online in July in the journal Neurobiology of Aging.

Developing drugs that slow the onset of Alzheimer's disease requires that the drugs be tested in clinical trials that run between 18 and 24 months, Rosa-Neto said. But if people who are selected for the trial never develop Alzheimer's during that time, it's impossible to say whether a drug was effective, he said.

"You want to include people who will be progressing from mild cognitive impairment to dementia in the time of the clinical trial," Rosa-Neto said. Alzheimer's disease is the most common form of dementia, according to the Alzheimer's Association.

But selecting the best patients for these trials is a challenge, because it is difficult to predict who will develop the condition, Rosa-Neto said. Scientists know that the buildup of a protein called amyloid, which accumulates in various regions of the brain, can lead to cognitive impairment. But piecing together the complex patterns of where and how much of the protein builds up, and then using that information to predict when a person will develop Alzheimer's disease is difficult to do by reading PET scans alone. (These scans are imaging tests that use a radioactive dye to identify certain diseases in the body.)

The presence of amyloid in the brain, however, doesn't necessarily mean that a person will develop Alzheimer's within a certain time; for some, it may take five to 10 years for the symptoms of dementia to appear, Rosa-Neto said. Others may never develop the disease, he said. But once a person has developed dementia, it is very difficult to return the brain to normal cognitive function, Rosa-Neto added.

The Alzheimer's-predicting algorithm

The artificial intelligence program that Rosa-Neto's team developed could help doctors identify the best participants for Alzheimer's drug clinical trials by predicting who is likely to develop the disease within a two-year window.

Creating an effective AI algorithm involves three main steps: writing the software, training it and then testing it to see how well it works, the researchers said.

As they were writing the software, the software engineers gave the algorithm some hints to help it analyze the PET images, Rosa-Neto said. The engineers designed it to take into consideration a common problem that pops up when studying people with mild cognitive impairment: In any given population, only a small fraction of a people will develop dementia.

The programmers also designed the algorithm to consider that the buildup of amyloid protein can occur at different rates, in different concentrations and at different locations in the brain, according to the study. [10 Things You Didn't Know About the Brain]

During the training portion of the study, the scientists used the algorithm to analyze the presence of amyloid in PET scans from nearly 200 patients who had mild cognitive impairment. The algorithm was then shown images from up to 24 months before the patients had developed the disease.

Once the program learned from this information, it was shown an entirely new set of amyloid PET brain scans from more than 270 individuals who had mild cognitive impairments. Of them, 43 were diagnosed with probable Alzheimer’s disease after the 24-month follow-up. However, the algorithm was shown only the images taken before the disease had fully developed. Using what it had learned, the AI algorithm predicted with 84 percent accuracy which individuals would develop the disease, according to the study.

In the study, the authorsnoted that no system that predicts Alzheimer’s disease based on images alone can be 100 percent accurate. In about 10 percent of diagnoses of “probable Alzheimer’s diseases,” for example, people actually have a different form of cognitive impairment.  

The researchers also noted the group of people included in the study described themselves as having some loss of memory and may not represent the general public. The authors added that it would be highly desirable to replicate the findings in a general population.

Based on this study, the team also created a pilot version of a real-time prediction tool that will analyze individuals' PET brain scans and spit out probabilities of when the individuals may develop dementia within a 24-month period. The tool is available to the public online.

Originally published on Live Science.

Consider it another strike against not getting enough sleep: A new study finds that getting too little REM sleep may be linked to a higher risk of dementia later in life.

REM, or "rapid eye movement," sleep is one of four sleep stages, which also include two stages of light sleep and a stage of deeper sleep called slow-wave sleep. REM sleep is characterized by vivid dreams and high levels of brain activity, similar to the brain's state when its awake. Humans typically cycle through several periods of REM sleep between the other stages of sleep each night.

In the new study, published today (Aug. 23) in the journal Neurology, researchers found that the people who developed dementia had gotten significantly less REM sleep when examined overnight years earlier compared with the people who didn't develop cognitive problems. [Get Better Sleep in 2017]

The study does not prove that low levels of REM sleep cause dementia; rather, it shows an association between the two, said lead study author Matthew Pase, a senior research fellow at Swinburne University of Technology in Australia.

Pase offered several ideas for how REM sleep and dementia might be linked.

"On one hand, REM may help protect connections within the brain that are vulnerable to damage with aging and Alzheimer's disease," Pase told Live Science. "On the other hand, perhaps lower REM is caused by other potential dementia risk factors, such as heightened anxiety and stress. This requires further study."

Doctors have long known that poor sleep can result in mental and emotional health problems. But details about which types of sleep are associated with dementia and long-term cognitive decline have been lacking. More than 10 percent of Americans over age 65 have some form of dementia, according to the Centers for Disease Control and Prevention.

In the new study, the researchers looked at more than 320 people in the U.S. whose average age was 67. These people were already part of an ongoing, larger study on heart health. The researchers collected sleep data approximately half way through the as they followed the participants for an average of 12 years. During that time, 32 people (about 10 percent) were diagnosed with some form of dementia; among those 32 people, 24 were diagnosed with Alzheimer's disease.

The people who developed dementia spent an average of 17 percent of their sleep time in REM sleep, compared with 20 percent for those who did not develop dementia. The researchers found that for every 1-percent reduction in REM sleep, there was a 9-percent increase in the risk of dementia. The results held up even after the researchers adjusted for other factors that could affect dementia risk or poor sleep, such as heart disease, depression and medication use.

Also, the time that the people spent in stages of non-REM sleep was not associated with dementia risk, the study found. [5 Surprising Sleep Discoveries]

"The study is valuable, since it has identified inadequate REM sleep as correlating with dementia risk," said Dr. Pinky Agarwal, a neurologist at EvergreenHealth in Washington and a professor of neurology at the University of Washington. Agarwal was not part of the study.

"The current [scientific] literature is mixed and mostly identifies inadequate 'slow wave sleep' [a type of deep, non-REM sleep] as a risk, but these have been much shorter-duration studies," Agarwal told Live Science. Because REM sleep is thought to be related to how the brain processes and retains memories, the new findings make sense, she said; dementia is, in part, marked by memory problems. The research points to the need for closer follow-up to recognize signs of dementia in patients with decreased REM sleep, she added.

Indeed, Pase noted that his research group would like to understand why a lower amount of REM sleep is tied to an increased risk of dementia. He hopes to tap into a larger sample of data to examine the relationship between sleep and signs of accelerated brain aging, such as poor thinking, memory problems and loss of brain volume.

This further research might provide more information about how getting less REM sleep, or even poor sleep in general, could lead to the development of dementia, Pase said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Country music legend Glen Campbell has died at age 81 following a long battle with Alzheimer's disease, his family announced today.

Campbell was diagnosed with Alzheimer's disease in 2011, at the age of 75, according to Rolling Stone. Later that year, he announced he was retiring because of his illness, and began a farewell tour that included 151 shows, Rolling Stone said.

Although Alzheimer's disease shortens people's life spans, it is usually not the direct cause of a person's death, according to the Alzheimer's Society, a charity in the United Kingdom for people with dementia. Rather, people die from complications from the illness, such as infections or blood clots.

Alzheimer's is a progressive brain disease in which abnormal protein deposits build up in the brain, causing brain cells to die. The illness is best known for causing memory loss, but it also has other debilitating effects on the body, and can affect people's ability to move and eat by themselves. There is no cure for the illness. [6 Big Mysteries of Alzheimer's Disease]

Alzheimer's patients may have difficulty swallowing, and they may inhale food, which can result in aspiration pneumonia, Dr. Marc L. Gordon, chief of neurology at Zucker Hillside Hospital in Queens, New York, who was not involved in Campbell's care, told Live Science in a 2014 interview. Pneumonia is listed as the cause of death in as many as two-thirds of deaths of patients with dementia, according to the Alzheimer's Society. 

Alzheimer's patients may also become bedridden, which can increase their risk of fatal blood clots, Gordon said.

Weight loss and other complications from Alzheimer's can also lead to a weakened immune system, according to the Alzheimer's Society. With a weakened immune system, the person can become more susceptible to potentially life-threatening infections, according to the National Institute on Aging.

These effects on the body are most pronounced in the advanced stages of the disease, which lasts about 1.5 to 2 years, on average, according to the National Institutes of Health.

Deaths from Alzheimer's disease are on the rise in the United States, according to a recent report from the Centers for Disease Control and Prevention (CDC). The report found that the rate of death from Alzheimer's disease increased by more than 50 percent, from about 16 deaths per 100,000 people in 1999 to 25 deaths per 100,000 people in 2014.

The number of people who died from Alzheimer's also more than doubled during this period, from 44,536 deaths in 1999 to 93,541 deaths in 2014.

The increasing number of deaths from Alzheimer's is partly due to the growing number of older adults in the United States, as Alzheimer's disease most commonly affects adults ages 65 years and older, the CDC researchers said.

But the rise in the rate of deaths from the disease may also be due to an increase among doctors, coroners and medical examiners specifically reporting Alzheimer's disease as a cause of death, the report said.

Still, overall, researchers may underestimate the true number of Alzheimer's deaths, since some doctors may report pneumonia or other complications as the cause of death, rather than Alzheimer's itself. A 2014 study estimated that as many as 500,000 people in the United States died from Alzheimer's in 2010.

Alzheimer's disease is the sixth-leading cause of death in the United States, according to the CDC.

Editor's note: Portions of this article were previously published on Live Science.

Original article on Live Science.

One-third of dementia cases could be prevented if more people could be helped to behave in ways that would improve their brain health, according to a new report.

Some public health strategies aimed at helping people to be healthy — for example, by staying in school past age 15, protecting their hearing in midlife and keeping up with exercise and hobbies in old age — could help to decrease the global numbers of dementia cases, the researchers said in their report, published today (July 19) in the journal The Lancet.

"Society must engage in ways to reduce dementia risk throughout life, and improve the care and treatment for those with the disease," study co-author Dr. Lon Schneider, a professor of psychiatry, neurology and gerontology at the University of Southern California, said in a statement. "This includes providing safe and effective social and health-care interventions in order to integrate people with dementia within their communities. Hopefully this will also ensure that people with dementia, their families and caregivers, encounter a society that accepts and supports them." [6 Big Mysteries of Alzheimer's Disease]

In the study, the researchers looked at previous research that has examined risk factors for dementia throughout people's lives. For example, they looked at studies that had examined the link between people's education, health, physical activity levels and the risk of dementia. The researchers then calculated and modeled the potential impact that reducing many different risk factors would have on the global prevalence of dementia.

The investigators found that targeting nine risk factors could slash the worldwide number of dementia cases by 35 percent. For example, if all young people continued their education past age 15, the number of dementia cases would be reduced by 8 percent, the researchers found. If all middle-age people with hearing loss were treated for the condition, the number of dementia cases would be reduced by 9 percent. And if all smokers older than 65 quit smoking, the number of dementia cases would be reduced by 5 percent, the researchers found.

The other six factors tied to dementia risk were high blood pressure and obesity in midlife, and the combination of depression, physical inactivity, social isolation and diabetes in people older than 65.

More research is needed to clarify exactly why and how each of these factors impacts a person's dementia risk, the researchers said. However, when it comes to the link between education and dementia, previous research has suggested that more education may increase a person's cognitive reserve — that is, the mind's resilience to brain damage that aging may inflict — the researchers said.

Smoking has a negative impact on the cardiovascular system, and previous research has linked cardiovascular problems with dementia, the researchers said.

Social isolation may lead to a decline in cognitive activity, which previous research has linked to accelerated cognitive decline, the researchers said. [6 Foods That Are Good For Your Brain]

The link between depression and dementia remains largely unclear, but one possible mechanism is that depression may affect the growth of brain cells and the volume of the hippocampus — a major brain component — thus upping the risk of dementia, the researchers said.

Further research is needed to understand the link between hearing loss and dementia, and to determine whether hearing aids may help to alleviate the impact of hearing loss on dementia risk, the researchers said.

The report had certain limitations, the authors said. For example, the authors did not consider diet and alcohol in their estimates, and these factors may also be a factor in people's dementia risk, according to the report.

Originally published on Live Science.

Deaths from Alzheimer's disease are on the rise in the United States, according to a new study from the Centers for Disease Control and Prevention (CDC).

Researchers at the CDC found that, in recent years, the rate of death from Alzheimer's disease increased by more than 50 percent, from about 16 deaths per 100,000 people in 1999 to 25 deaths per 100,000 people in 2014.

And the number of people who died from Alzheimer's more than doubled during this period, from 44,536 deaths in 1999 to 93,541 deaths in 2014.

The increasing number of deaths from Alzheimer's is partly due to the growing number of older adults in the United States, as Alzheimer's disease most commonly affects adults ages 65 years and older, the CDC researchers said.

But the rise in the rate of deaths from the disease may also be due to an increase among doctors, coroners and medical examiners specifically reporting Alzheimer's disease as a cause of death, the researchers said.

The report also found that the percentage of Alzheimer's deaths that occurred at home, rather than in a nursing home or hospital, increased during the study period, suggesting that there has been a rise in the number of people caring for those with the disease. [6 Big Mysteries of Alzheimer's Disease]

"Millions of Americans and their family members are profoundly affected by Alzheimer’s disease," Dr. Anne Schuchat, the acting director of the CDC, said in a statement. "As the number of older Americans with Alzheimer's disease rises, more family members are taking on the emotionally and physically challenging role of caregiver than ever before. These families need and deserve our support," Schuchat said.

Alzheimer's is a progressive brain disease in which abnormal protein deposits build up in the brain, causing brain cells to die. The illness is best known for causing memory loss, but it also has other debilitating effects on the body, possibly affecting people's ability to move and eat by themselves. There is no cure for the illness.

The disease is usually not the direct cause of a person's death, according to the Alzheimer's Society, a charity in the United Kingdom. Rather, people die due to complications from the illness, such as infections (including pneumonia) or blood clots.

Still, the new findings might underestimate the true number of Alzheimer's deaths, since some doctors may report pneumonia or other complications as the cause of death, rather than Alzheimer's itself.

Caregivers for Alzheimer's patients may benefit from learning about the stages of the disease and how to cope with the challenges of caregiving, as well as from home health assistance or caregiver support groups, according to the National Institute on Aging.

"Supportive interventions can lessen the burden for caregivers and improve the quality of care for people with Alzheimer's disease," said study co-author Christopher Taylor, an epidemiologist at the CDC's National Center for Chronic Disease Prevention and Health Promotion.

The study is published today (May 25) in the CDC journal Morbidity and Mortality Weekly Report.

Original article on Live Science.

The irreverent, surreal style of humor in the "Monty Python" movies and TV series came, in part, from comedian Terry Jones, a member of the comedy troupe. But now, The Guardian has reported that Jones, who is 75, has a little-known form of dementia.

Jones was diagnosed in 2015 with a condition called frontotemporal dementia, The Guardian reported on Sunday (April 16).

But what is this type of dementia? And how does it affect the brain? [10 Things You Didn't Know About the Brain]

Dementia is a general term for a condition in which changes in a person's brain affect his or her ability to carry out everyday activities, according to the Mayo Clinic.

Although frontotemporal dementia may sound unfamiliar, it's in fact the second most common type of dementia, after Alzheimer's disease, in people under 65, according to the National Institute on Aging (NIA). About 10 percent of people with dementia have frontotemporal dementia, the NIA says. People with frontotemporal dementia typically develop the condition at a younger age, between 40 and 45, than people with Alzheimer's develop that disease, the Mayo Clinic says.

There are several types of frontotemporal dementia, but all affect parts of the brain called the frontal and temporal lobes, the NIA says. When a person has  the disease, nerve cells in the frontal and temporal lobes become damaged and die, the NIA says. As this happens, these regions of the brain shrink.

Indeed, Jones described the disorder by saying, "My frontal lobe has absconded," according to The Guardian.

These regions of the brain are responsible for functions including planning, managing emotional responses, language skills and movement, according to the NIA. People with frontotemporal dementia experience symptoms related to these functions, with changes in their behavior, language abilities and movement, according to the University of California, San Francisco.

Which symptoms appear first depends on the part of the brain that is affected, the NIA says. For example, if the disease starts in the part of brain responsible for decision-making, a person's first symptom may be trouble managing money, the NIA says. 

Jones' first symptoms occurred when he had trouble remembering his lines during a performance in London in 2014, The Guardian reported.

Extreme changes in behavior and personality are also common signs and symptoms of the disease, according to the Mayo Clinic. These changes can include increasingly inappropriate actions, loss of empathy, and lack of judgement and inhibition, the Mayo Clinic says.

The cause of frontotemporal dementia in an individual is usually unknown, according to the Mayo Clinic. Although the disease has been linked to several genetic mutations that can be inherited, more than half of the people who develop the disease have no other family members with the condition, the Mayo Clinic says. 

Originally published on Live Science.

Antioxidant supplements may not help ward off dementia, a new study suggests. Although previous research had suggested a possible link between the two, this latest study is one of the largest studies to investigate whether antioxidants could help ward off dementia, and found no such link.

Researchers analyzed information from more than 7,500 U.S. men ages 60 and older who were randomly assigned to take a daily vitamin E supplement, a daily selenium supplement, both supplements or a placebo. Both vitamin E and the mineral selenium are antioxidants, which means they may prevent some types of damage in cells.

The men took the supplements for about five years, on average, and during that time, the researchers followed up with them to determine which men developed dementia. After that, a subset of about 3,700 men agreed to be followed for an additional six years while they were not taking the supplements.

The study found that the rate of dementia was about the same among men who had taken the supplements for five years and those who had taken the placebo during that time. In each of the four study groups, between 4 and 5 percent of the men developed dementia during the study. [6 Big Mysteries of Alzheimer's Disease]

"The supplemental use of vitamin E and selenium did not forestall dementia," and these supplements are not recommended to prevent dementia, the researchers, from the University of Kentucky, concluded in their paper, which was published today (March 20) in the journal JAMA Neurology.

Antioxidants are thought to thwart a damaging process called oxidative stress, which is implicated in the development of dementia. Some previous studies suggested that antioxidants might improve people's cognition or reduce their risk of dementia, but subsequent studies that were more rigorously designed — including this most recent study — have failed to find a link.

However, the new study had limitations that could have affected the results, the authors said. For example, the data on the participants in the new study actually came from a larger study that looked at whether vitamin E or selenium could prevent prostate cancer, called SELECT (which stands for "Selenium and Vitamin E Cancer Prevention Trial"). But that study ended in 2009, when an analysis failed to show a benefit of the supplements, and subsequent studies suggested that vitamin E may even increase the risk of prostate cancer. When the SELECT study ended, many of the participants dropped out, and the researchers involved in the new study lost about half of their participants.

In addition, the dementia screening test used in the study might have missed some people who were in the early stages of dementia, the researchers said.

Also, most of the participants were in their 60s during the study period, and the risk of dementia is still low for people in this age group, said Dr. Steven DeKosky, of the University of Florida, and Dr. Lon Schneider, of the University of Southern California, who were not involved in the research and wrote an editorial accompanying the new study in the journal.

Original article on Live Science.

Keeping your heart healthy could also benefit your brain, hints a new study suggesting that people who have risk factors for heart disease in middle age are also at increased risk for dementia later in life.

The study analyzed information from more than 15,000 U.S. adults who started the study when they were ages 45 to 64 and were followed for 25 years. During the study, about 1,500 participants developed dementia.

People who had diabetes or high blood pressure at the start of the study, or who smoked at that time, were at increased risk for developing dementia about 25 years later. (All three of these factors are known to increase the risk of heart disease.) [6 Big Mysteries of Alzheimer's Disease]

Specifically, those with diabetes in middle age were 77 percent more likely to develop dementia during the study, compared to those without diabetes in middle age. Those who smoked at the start of the study were 41 percent more likely to develop dementia than those who didn't smoke at the start of the study. And those who had high blood pressure were 39 percent more likely to develop dementia than those who didn't have high blood pressure.

"The health of your vascular system in midlife is really important to the health of your brain when you are older," study researcher Dr. Rebecca Gottesman, an associate professor of neurology and epidemiology at Johns Hopkins University in Baltimore, said in a statement. "If you want to protect your brain as you get older, stop smoking, watch your weight, and go to the doctor so diabetes and high blood pressure can be detected and treated," Gottesman said.

Dementia refers to a group of symptoms — such as memory loss and problems with communication — that result from changes in the brain. There are many diseases and conditions that can cause dementia, including Alzheimer's disease.

A growing body of evidence suggests that the risk of dementia is increased by conditions that damage the heart or blood vessels, such as high blood pressure, diabetes and stroke, according to the Alzheimer's Association.

The researchers note that the new study did not test whether treating heart disease risk factors actually lowers dementia risk. To take a look at exactly how these factors may increase the risk of dementia, more research is needed, the researchers said.

The study was presented today (Feb. 22) at the American Stroke Association's International Stroke Conference 2017 in Houston.

Original article on Live Science.

Updated on June 6, 2018

In a documentary filmed before his death, David Cassidy told producers he had "no sign" of dementia, according to Reuters. Instead, the actor said he had liver disease due to alcoholism, and that he had lied about giving up drinking. Cassidy died of liver failure on Nov. 21, 2017, according to the Washington Post.

Live Science published this article (below), on Feb. 21, 2017:

Actor and singer David Cassidy recently revealed he has dementia, but what exactly does this term mean?

Cassidy, who is 66, told People magazine on Monday (Feb. 20) that he has dementia, and will stop touring as a musician because of his diagnosis. The actor also said that both his mother and grandfather suffered from dementia.

"I was in denial, but a part of me always knew this was coming," Cassidy said.

Dementia is not a specific disease, but rather a group of symptoms resulting from changes in the brain that affect people's ability to carry out everyday activities, according to Mayo Clinic. These symptoms can include memory loss, problems with communication (such as trouble engaging in conversation), difficulty solving problems and reasoning, or changes in personality. Dementia is caused by damage to the brain's nerve cells, and the types of symptoms people have can depend on the part of the brain that's affected, according to Mayo Clinic. [6 Big Mysteries of Alzheimer's Disease]

Doctors diagnose dementia when people have impairments in at least 2 out of 5 core brain functions, according to the Alzheimer's Association. These five core functions are memory, communication and language, ability to focus, reasoning and judgment, and visual perception (such as the ability to judge distance or determine the height of a stair).

People's risk for dementia increases as they get older, and those over age 65 are at particularly high risk, according to Mayo Clinic. Those with a family history of dementia are also at greater risk for the condition.

There are many diseases and conditions that can cause dementia, including the following:

Alzheimer's disease. This is the most common type of dementia, accounting for up to 80 percent of dementia cases, according to the Alzheimer's Association. A hallmark of Alzheimer's disease in the brain is the buildup of proteins known as beta-amyloid and tau.

Vascular dementia. This is the second most common type of dementia, accounting for about 10 percent of cases, according to the Alzheimer's Association. It is caused by damage to the brain's blood vessels, which can occur after a stroke.

Lewy body dementia. Abnormal clumps of a protein called alpha-synuclein cause this type of dementia, according to the Alzheimer's Association. In addition to memory loss, people with Lewy body dementia may also experience sleep disturbances, visual hallucinations and problems with movement. After his death in 2014, actor Robin Williams was found to have Lewy body dementia.

Parkinson's disease. People with Parkinson's disease often experience symptoms of dementia as the disease progresses. It is caused by the breakdown of nerve cells that produce a brain chemical called dopamine.

Frontotemporal dementia. This is a group of dementias that involves the breakdown of nerve cells in the brain's frontal and temporal lobes, according to Mayo Clinic. It can cause changes in personality and behavior. People with this type of dementia generally start showing symptoms at younger ages (around age 60), according to the Alzheimer's Association.

Mixed dementia. This occurs when people have the brain abnormalities of several different types of dementia at the same time. For example, people may have brain abnormalities linked with Alzheimer's disease, vascular dementia and Lewy body dementia.

Most dementias are progressive disorders, which means the symptoms get worse over time. But some symptoms of dementia are reversible. For example, thyroid problems, exposure to heavy metals and reactions to certain medications can cause symptoms of dementia that are reversed with treatment, according to Mayo Clinic.

Cassidy did not specify which type of dementia he has. But he has spoken at events for the Alzheimer's Foundation of America in order to raise awareness about dementia, according to AgingCare.com. His mother, Evelyn Ward, died from an Alzheimer's-related dementia, according to the Hollywood Reporter.

Original article on Live Science.

Some older people who have signs of Alzheimer's disease in their brains may actually have pretty good memories, a small new study suggests.

In the study, researchers examined the brains of eight people who had died at ages 90 and older from various causes and found that some of them had signs of Alzheimer's disease. However, tests of their cognitive function that were conducted shortly before their death showed that these people had memories that were as good as those of healthy people who were 30 to 40 years younger.

The results suggest that some individuals with Alzheimer's disease may be protected against some of its symptoms, like memory problems, said lead study author Changiz Geula, a professor of cognitive neurology at Northwestern University Feinberg School of Medicine in Chicago, Illinois. [6 Big Mysteries of Alzheimer's Disease]

It is not clear why some people's brains and memories seem to be protected against such symptoms, but the researchers suspect that genetic and environmental factors may be at work, Geula told Live Science.

The eight people in the study were initially part of a larger study of individuals who died in their 90s and whose cognitive function was examined shortly before their death. The study participants also agreed to donate their brains to science after their death.

Based on the results of the cognitive-function tests that were conducted among the larger group before death, the researchers selected and looked at the brains of eight people whose memories were as good as those of healthy 50- to 60-year-olds. They detected physical signs of Alzheimer's disease, such as plaques and tangles, in three of those brains.

However, when the researchers examined the nerve cells in the hippocampus — a brain area that's associated with forming memories — it turned out that, in the brains of the three people with the good memory abilities, the cells in this area looked relatively normal. This is unusual for people who have the plaques and tangles in the brain that signify Alzheimer's disease, the researchers said. Usually, in people whose brains show evidence of plaques and tangles, the number of nerve cells in the hippocampus is reduced, Geula said.

This finding, which indicates that the nerve cells in the three people with superior memories have somehow been preserved, suggests that the preservation of these cells might be one of the factors that helps to protect these people's memories, Geula said. However, its not clear that the preserved nerve cells were the cause of the people's good memory abilities — it's also possible that some other factor was responsible. [You Forget: 5 Strange Facts About Memory]

Moreover, if the preservation of these nerve cells is involved having a superior memory, it is likely not the only protective mechanism, he said. The researchers said that they think that certain genetic factors may also help to protect some people's brains against the symptoms of Alzheimer's disease.

It is also possible that a person's diet or the amount of time he or she spends exercising may help to protect the brain against Alzheimer's, although more research is needed before researchers can know whether this is true, Geula said.

Future research is also needed to confirm the new findings in a larger sample of people, he said.

Originally published on Live Science.

The American population is getting older, but the percentage of U.S. seniors with dementia is actually declining, a new study found.

In the study, the researchers analyzed information from a nationally representative sample of about 21,000 U.S. adults ages 65 and older who were tested for dementia from 2000 to 2012. (About 10,500 people were tested in 2000, and 10,500 were tested in 2012; about 4,000 of the participants were tested in both of those years.)

In 2000, 11.6 percent of older adults had dementia, but that number dropped to 8.8 percent by 2012, the researchers found.

Although some previous U.S. studies had suggested the prevalence of dementia in the U.S. was declining in recent years, those studies were not representative of the entire U.S. population, the researchers in the new study said.

The new findings "add to a growing body of evidence that this decline in dementia risk is a real phenomenon, and that the expected future growth in the burden of dementia may not be as extensive as once thought," Dr. Kenneth Langa, the lead author of the study and a professor at the University of Michigan's Institute for Social Research and School of Public Health, said in a statement.

Dementia is not a specific disease, but rather a group of symptoms, which can include problems with thinking and solving problems, as well as personality changes, according to the National Institutes of Health. [6 Big Mysteries of Alzheimer's Disease]

The risk of developing these symptoms has also been linked toother factors, like education, the new study suggested. Researchers found that the people in the study who had more years of education had a lower risk of dementia. Those with 16 years or more of education were about 70 percent less likely to have dementia, compared with those who had less than 12 years of education. During the study period, the average number of years of education among participants increased from 12 to 13 years.

More years of education may help protect against dementia in a number of ways, the researchers said. Spending more years in school may help the brain's "cognitive reserve," meaning the brain may be better able to compensate for abnormalities that occur in older age.

Having more years of education can also allow people to obtain more cognitively challenging jobs, which could also help protect the brain, the researchers said. And people who have more years of education may also be more likely to exercise and eat healthy, and less likely to smoke, which are all behaviors that are linked with better brain health.

Interestingly, the researchers noted that the drop in dementia prevalence occurred despite increases in the rates of certain conditions that can increase the risk of dementia: diabetes, high blood pressure and obesity. The researchers said they suspect that better treatment of cardiovascular disease and diabetes may have also contributed to the decline in dementia.

Still, more research is needed to identify all the factors contributing to the decline in dementia prevalence, the investigators said.

The researchers noted that, despite the decline seen in the study, dementia will still be a very important health issue in years to come.

"It does nothing to lessen the impact that each case has on patients and caregivers. This is still going to be a top-priority issue for families, and for health policy, now and in the coming decades," Langa said.

Original article on Live Science.

If you've ever felt a rush of dizziness after standing up too quickly, take heed: Older adults who experience that disorienting feeling frequently may be more likely to develop dementia, a new study from the Netherlands finds.

In the study, researchers found that older adults who had "orthostatic hypotension," a condition in which blood pressure drops whenever they stand up suddenly, were 15 percent more likely to develop dementia later in life.

The dizzy feeling, sometimes referred to as a "head rush," occurs because standing up quickly triggers a sudden drop in blood pressure, which, in turn, decreases blood flow to the head, according to the study, published today (Oct. 11) in the journal PLOS Medicine. 

The research included more than 6,200 men and women who were enrolled in the Rotterdam Study. At the study's start, the participants were 69 years old, on average, and they did not have dementia and had never had a stroke. When the study began, the researchers noted which of the people in the study had orthostatic hypotension. [10 Ways to Keep Your Mind Sharp]

After an average of 15 years of follow-up, the researchers found that orthostatic hypotension was associated with a 15 percent increased risk of all types of dementia, including Alzheimer's disease, vascular dementia and Parkinson's dementia.

Normally, the heart compensates for a sudden drop in blood pressure by beating faster to supply more blood to the body, according to the study. But people with orthostatic hypertension who did not have this "compensatory" increase in heart rate were 39 percent more likely to develop dementia compared with people who did not have orthostatic hypotension, according to the study.

The researchers, led by Dr. Frank Wolters, an epidemiologist at the Erasmus Medical Center in the Netherlands, noted that the study does not prove cause and effect but rather that it shows an association between orthostatic hypotension and dementia risk.

There are possible explanations for this link. For example, if blood flow to the head decreases every time a person stands up, the brain may not get enough oxygen, which could lead to brain damage, the researchers wrote.

In addition, several previous studies also suggested a link between reduced blood flow to the brain and dementia risk, the researchers wrote.

Originally published on Live Science.

The mysteries of Alzheimer's

Despite intensive, worldwide research efforts for more than three decades to better understand Alzheimer's disease, there are still numerous mysteries surrounding the condition.

Alzheimer's disease is a slowly progressing brain disorder. In people with the condition, abnormal deposits of a protein called amyloid-beta forms sticky plaques in the brain, and strands of the protein tau twist around, causing tangles that ultimately kill brain cells and cause a loss of memory, thinking and reasoning skills.

About 5.4 million Americans currently have Alzheimer's disease, and the number is expected to grow rapidly in the coming years as a larger share of the population ages, according to the Centers for Disease Control and Prevention. [7 Ways to Prevent Alzheimer’s Disease]

Researchers are now aiming to better understand what underlies the disease, as well as improving methods of detection, prevention and treatment. 

In the past 15 years, biomarkers (biological markers), including new brain-imaging techniques such as Positron Emission Tomography (PET) scans, and new methods to analyze cerebrospinal fluid have helped researchers to detect early changes in brain function in people with Alzheimer's, said Dr. John Morris, a professor of neurology and director of the Knight Alzheimer's Disease Research Center at Washington University School of Medicine in St. Louis.

For example, using radioactive tracers that can bind with amyloid protein deposits in plaque and tau protein in neurofibrillary tangles, researchers can now use PET scans to peer inside the brain to detect whether Alzheimer-related changes are present, Morris said.

In addition, they can perform a spinal tap to withdraw a sample of cerebrospinal fluid, and use it to measure whether a person has low concentrations of amyloid beta protein and high concentrations of tau protein, which have both been linked with a diagnosis of Alzheimer's disease, he told Live Science.

Despite these advances, there are many aspects of  Alzheimer's disease that researchers only partially understand, said Dr. Dennis Selkoe, co-director of the Ann Romney Center for Neurological Diseases at Brigham and Women's Hospital in Boston, who has been conducting research to uncover the causes of Alzheimer's disease for more than 30 years.

For people with Alzheimer's disease and their loved ones, the most important mystery to solve is finding a safe and effective treatment for this neurodegenerative disorder, Selkoe said.

Here are the six biggest mysteries of Alzheimer's disease, according to these two researchers, and a look at the work that's being done to solve them.

Mystery: What will be a safe and effective treatment for Alzheimer's disease?

Although this is not a complete mystery because many clinical trials of experimental treatments are underway, researchers are working hard to find a safe and effective treatment to slow down Alzheimer's, or even prevent it from developing, Selkoe said.

Selkoe has helped pioneer extensive research on the "amyloid hypothesis," the idea that an imbalance between the production and removal of a protein called amyloid beta in the brain is what triggers Alzheimer's disease.

There are certain "sticky" amyloid proteins that build up and form plaque in the brain that can short-circuit cells involved in memory, Selkoe said. It's possible that if there were therapies that could control or reduce the accumulation of this plaque, people would not become forgetful, he said.

Selkoe said that he was encouraged by the results of a recent investigational trial of a drug called aducanumab, which is an antibody-based immunotherapy. The drug was given intravenously every month for one year to 165 people with early or mild Alzheimer's disease, who had evidence of plaque buildup in the brain.

Within six months, participants taking the drug began to show declines in the amount of amyloid beta plaque, compared with those taking a placebo. By one year, more clearing of amyloid beta had occurred, according to the study findings reported in August in the journal Nature. The researchers found that there appeared to be a slowing of cognitive decline in a dose-dependent manner, meaning that the patients who were given higher doses showed a greater degree of slowing. [7 Ways the Mind and Body Change With Age]

Participants taking the drug didn't get better, but there was a stabilization of the disease's progression, Selkoe told Live Science. As for the drug's safety, about 30 percent of participants experienced a short-term change in the balance of the watery fluid in the brain, a side effect that went away by itself during the trial, and a few people had headaches, he said.

For now, this antibody-based therapy looks effective and appears safe, and a larger trial of this drug and other antibody-based treatments is underway, Selkoe said.

Mystery: Why have clinical trials of some highly promising drugs failed to show positive results?

One reason for the discouraging results of some high-profile clinical trials of promising therapies over the last 15 years is that they included people who may not have had Alzheimer's disease. Because of an imperfect testing process, some participants may have been included in these trials who had symptoms similiar to Alzheimer's but actually had another form of dementia, Morris told Live Science. Now, people in experimental drug trials need to test positive for biomarkers of Alzheimer's disease before they can participate in the research, he said.

Another reason the drugs did not appear to work in the trials could have been that the participants' disease was too far advanced, Morris said. By the time symptoms of declining thinking and memory skills appear in older adults, the brain has already been damaged by plaques and tangles, and there has been a loss of brain cells, he said.

Now that biomarkers can better identify which older adults should be in drug trials, researchers could introduce experimental medications in people at earlier stages of the disease — years or decades before symptoms appear — to see if the medicines might slow down or halt the Alzheimer's disease process in the brain, Morris said. 

Mystery: How do brain cells die once amyloid plaque gets deposited?

Many aspects of the disease process underlying Alzheimer's remain unclear to researchers. But it's possible that the disease begins with the abnormal metabolism of amyloid plaque in the brain that sets off a toxic cascade of events, Morris said. These events may activate immune system cells that trigger inflammation, or there could be some other type of injury to brain cells, he explained.

Because of the many wide-ranging brain changes caused by the disease, treatment may someday involve the use of multiple drugs that target different aspects of the Alzheimer's disease process, not just the buildup of amyloid deposits in the brain, Morris said.

In fact, some researchers suspect it's unlikely that there will be a single drug treatment for Alzheimer's disease. It's more probable that there will be a cocktail of medications, like the treatments used to successfully treat AIDS and some cancers, which are aimed at several different targets. These medications could target the underlying disease itself, as well as stopping or delaying damage to the brain cells that worsens its symptoms. 

Mystery: What is the relationship between the plaques and the tangles found in the brain?

Since 1906 when the disease was first described by Alois Alzheimer, researchers have known about the presence of plaques and tangles in the brains of people with Alzheimer's. But one of the big mysteries of the disease is how these two hallmarks of the disease might be related, Selkoe said.

Scientists have unraveled part of the answer to this mystery by discovering that the plaques develop in the brain first, before the tangles, Selkoe told Live Science. It's also known that the buildup of amyloid beta protein causes injury to nerve cells, and that strands of tau protein twist and form tangles inside nerve cells, he said.

But researchers don't yet know exactly how these plaques and tangles affect brain function, eventually leading to the memory problems, behavioral changes and other symptoms of Alzheimer's disease. Selkoe said. And they also don't know whether amyloid in plaque and tau in tangles work separately, or together, to damage nerve cells, he added.

These are some reasons why therapies aimed solely at reducing amyloid buildup might not be enough by itself to treat Alzheimer's disease, and why there may also be a need for a drug that helps lower tau levels, Selkoe said. 

Mystery: What does inflammation have to do with Alzheimer's disease?

Another characteristic brain abnormality of Alzheimer's disease is inflammation — meaning the excessive action of the immune cells in the brain.

It's unclear whether inflammation is a result of having Alzheimer's disease, or whether the inflammatory process plays a role in its development. It's also possible that inflammation is both a cause and effect of the disease. [3D Images: Exploring the Human Brain]

What's known is that there are immune cells in the brain known as microglia that are normally present to clean up infections, which helps protect the brain, Selkoe said. There is also good evidence that these immune cells get upset about the buildup of too much amyloid in the brain, which makes them aggravated, causing the microglia to release too much protein, he said.

The release of too much protein by microglia can cause trouble at the synapses, or connections, between nerve cells, Selkoe said.Scientists wonder whether drugs aimed at controlling inflammation in the brain could also help control memory problems, he said.

Mystery: Why are certain regions of the brain more vulnerable to Alzheimer's disease?

"There is a lot that researchers don't understand about how Alzheimer's disease is manifested in a particular person," Morris said.

Not everyone has memory problems initially: Some people first develop changes in their behavior, such a a lack of empathy or a loss of inhibition, while others may have language difficulties, such as problems expressing themselves with language or hesitatating when they are speaking because they can't find the right words, Morris said. Still others may have problems interpreting visual stimuli, and complain of blurred vision or difficulty reading and writing, he said.

Scientists don't know why people have different presentations of the disease, although it usually first affects short-term memory, such as learning new information, and it typically involves forgetfulness, Morris said. It's unclear what causes certain brain regions to be affected first by the disease, while many other brain regions, by and large, are still functioning normally, he said. 

As Alzheimer's disease progresses, regions of the brain beyond those involved in memory and thinking become impaired, and in advanced stages, a person ends up with widespread brain disease, Morris said. The use of biomarkers is allowing scientists to see which regions of the brain are being targeted in the early stages of the disease, he said.

Originally published on Live Science.

In people with Alzheimer's disease, a new investigational drug can dramatically reduce the amount of amyloid beta plaque, the tangled clumps of proteins that form in the brains of Alzheimer's patients, according to a new early study of the drug.

The drug works by spurring the immune system to recognize and clear the plaques.

"We believe that's a hint of efficacy," study co-author Dr. Alfred Sandrock, a neurologist and an executive vice president at Biogen, said during a news briefing. "We believe that needs to be confirmed with further studies." Biogen is the Cambridge, Massachusetts, company that funded the trial and applied to patent the drug. [10 Things You Didn't Know About the Brain]

However, the study was too small to show whether there was an effect on the patients' symptoms of Alzheimer's disease. And the drug can also cause fluid accumulations in the brain in some genetically susceptible people, the researchers reported today (Aug. 31) in the journal Nature.  

Cause of dementia

Alzheimer's disease is the leading cause of dementia, affecting more than 5 million people in the United States, according to the Centers for Disease Control and Prevention. The hallmark of the disease is aggregation of an abnormal protein called amyloid beta, which looks like clumps of tangled fibrils on brain scans. Many scientists believe the amyloid beta fibrils are toxic to brain cells and are directly responsible for the memory loss, mood changes and loss of function that occur as the disease progresses, according to the paper. 

There is no cure for Alzheimer's, and the few treatments on the market have only modest, transient benefits.

Targeting amyloid beta

To find a better treatment, Sandrock and his colleagues at Biogen turned to older people who do not have dementia or Alzheimer's. They analyzed the chemicals present in healthy older people with no cognitive decline, as well as people whose cognitive decline had progressed very slowly. The team identified one immune compound, and made a drug that mimicked it, called aducanumab. In earlier animal studies, the drug seemed to target amyloid beta and spur other structures in the brain to engulf and clear the plaques, Sandrock said.

In the new study, researchers gave 165 patients with mild Alzheimer’s monthly infusions of either aducanumab or a placebo, and did a series of brain scans. The people taking aducanumab showed a sharp decrease in the amount of amyloid beta in their brains. The higher the dose of aducanumab they received, the greater the amyloid clearance revealed in magnetic resonance imaging (MRI) scans.

"After one year, you can see no red on the image, meaning the amyloid has almost completely disappeared," said Dr. Roger Nitsch, a co-author of the study and the director of the Institute for Regenerative Medicine at the University of Zurich. He is also a founder of the biopharmaceutical company Neuroimmune.

However, people who took the drug, and also carried a genetic change called the APOE gene variant, which is linked with Alzheimer's disease, were also more likely to experience a potentially dangerous side effect known as amyloid-related imaging abnormalities, or ARIA. This side effect showed up in brain scans as small pockets of fluid in the brain.

Although most people in the study who developed ARIA were asymptomatic, a few patients reported headaches. Studies in other Alzheimer's drug candidates have shown that in rare cases, ARIA can increase the risk of stroke or cerebral hemorrhage, the researchers said. ARIA, if it does occur, usually shows up early in treatment and can be managed and cleared by lowering the drug dose, Sandrock said.  

Cognitive benefits unclear

The study was not designed to show whether the drug can actually produce cognitive benefit; however, the team found hints of cognitive benefit that did not reach statistical significance.

"We're encouraged that, there appeared to be a slowing of cognitive decline at a dose-dependent manner, and also a dose-dependent slowing in functional decline," said study co-author Dr. Stephen Salloway, a neurologist at Butler Hospital in Providence, Rhode Island.

Much larger follow-up studies are needed to confirm that the benefit is real, Salloway said.

Indeed, the larger question is whether clearing amyloid beta will lead to dramatic improvements in cognitive decline, Dr. Eric Reiman, a psychiatrist and researcher at Banner Alzheimer's Institute, a research and patient care center in Phoenix, wrote in an editorial accompanying the new study in the journal. Some researchers believe beta amyloid is a byproduct of the destructive brain process, and not the cause, noted Reiman, who was not involved in the new study.

If larger trials of the drug show improvement in patients' cognitive function, that will help settle the debate on whether amyloid beta causes Alzheimer's, Reiman said.

"It would be prudent to withhold judgment about aducanumab's cognitive benefit until results from the larger trials are in," Reiman wrote in the article.

What's more, by the time people begin to show symptoms, it's thought that they have been accumulating plaque for 15 years and much of the cognitive damage may have already occurred, Sandrock said.

So eventually, this drug or another one like it, could be most effective when people first show signs of plaque accumulation, but have no cognitive symptoms, he speculated.

"I still think that treating early is going to be the key," Sandrock said.

Original article on Live Science.

Legendary comedic actor Gene Wilder has died at age 83 from complications of Alzheimer's disease, his family announced today. But what exactly does it mean to die from Alzheimer's?

Although Alzheimer's disease shortens people's life spans, it is usually not the direct cause of a person's death, according to the Alzheimer's Society, a charity in the United Kingdom for people with dementia. Rather, people die from complications from the illness, such as infections or blood clots.

Alzheimer's is a progressive brain disease in which abnormal protein deposits build up in the brain, causing brain cells to die. The illness is best known for causing memory loss, but it also has other debilitating effects on the body, and can affect people's ability to move and eat by themselves. There is no cure for the illness.

Alzheimer's patients may have difficulty swallowing, and they may inhale food, which can result in aspiration pneumonia, Dr. Marc L. Gordon, chief of neurology at Zucker Hillside Hospital in Queens, New York, who was not involved in Wilder's care, told Live Science in a 2014 interview. Pneumonia is listed as the cause of death in as many as two-thirds of deaths of patients with dementia, according to the Alzheimer's Society. [Top 10 Leading Causes of Death]

Alzheimer's patients may also become bedridden, which can increase their risk of fatal blood clots, Gordon said.

Weight loss and other complications from Alzheimer's can also lead to a weakened immune system, the Alzheimer's Society says. This increases a person's susceptibility to potentially life-threatening infections, according to the National Institute on Aging.

These effects on the body are most pronounced in the advanced stage of the disease, which lasts about 1.5 to 2 years, on average, according to the NIH.

Alzheimer's disease is the sixth-leading cause of death in the United States, according to the Centers for Disease Control and Prevention. In 2013, nearly 85,000 people in the United States died from the disease, the CDC says.

However, deaths from Alzheimer's disease may be underestimated, because death certificates often list pneumonia or another complication as the cause of death, rather than the underlying Alzheimer's, according to a 2014 study. The study estimated that as many as 500,000 people in the United States died from Alzheimer's in 2010.

Editor's note: Portions of this article were previously published on LiveScience.

Original article on Live Science.