Scientists have pinpointed the brain network that's involved in stuttering, brain scans reveal. 

The work suggests that stuttering may be triggered by disruption to a specific network of brain cells, or neurons that connects three major regions of the brain. These regions — the amygdala, the putamen and the claustrum — are respectively involved in regulating emotions, controlling movements and relaying information between different areas of the brain.

The brain imaging results were described in a recent paper, published May 27 in the journal Brain. 

Knowing what causes stuttering could aid the development of new targeted treatments for the condition, Dr. Juho Joutsa, co-senior study author and a professor of neurology at the University of Turku in Finland, told Live Science. Such treatments could include the use of electrical brain stimulation, which involves placing electrodes on or inside a patient's head and delivering pulses of electricity to target areas of the brain at specific times. 

Related: Super-detailed map of brain cells that keep us awake could improve our understanding of consciousness 

Finding a new target for treatment

Stuttering is a speech disorder that affects around 1% of adults and between 5% and 10% of children. The condition causes people to involuntarily repeat or prolong certain sounds, syllables and words as they speak, as well as experience "blocks" in speech. People who stutter can therefore experience difficulty in communicating with others, which can contribute to social anxiety. 

There are two major types of stuttering: developmental stuttering, which emerges in childhood but resolves before age 18 in up to 90% of cases, and the less-common, acquired form of stuttering, which can occur after a brain injury. These injuries include those caused by a stroke, or a disease such as Parkinson's.

Stuttering is typically treated with speech therapy. However, the benefits of this treatment do not always last, and there are currently no effective drugs to treat the condition. 

Until now, scientists didn't know where in the brain stuttering originated, which limited their ability to come up with alternate treatments. 

To find answers, Joutsa and colleagues started by looking at published medical case reports from 20 people who'd started stuttering after a stroke. They compared these reports to those from nearly 170 stroke patients at Turku University Hospital in Finland who did not develop stuttering. The team found that, in those who started stuttering, the damage caused by their strokes showed up in different parts of the brain but all clustered in the same brain network. The people who didn't develop stuttering didn't show this pattern.

The team uncovered this same pattern in a separate experiment in which they used magnetic resonance imaging (MRI) to scan the brains of 20 people who had developed stuttering after a stroke. 

Related: A mysterious brain network may underlie many psychiatric disorders

To determine if this brain network might indeed be responsible for all types of stuttering, and not just those caused by brain damage, the team also imaged the brains of 20 adults with developmental stuttering. In addition to scanning participants' brains, the researchers assessed the severity of their stuttering symptoms through video-recorded conversations and a questionnaire that the participants filled out. 

They uncovered patterns in how the participants' symptom severity related to the structure of their gray matter, which includes the main bodies of neurons. People more severely impacted by their stuttering showed higher gray matter volume in the same brain network linked to stuttering after stroke. This correlation was consistent in that, the greater the volume someone showed in the network, the more severe their stuttering was. 

Taken together, these findings suggest that there is a common brain network underlying stuttering, regardless of its original trigger. 

This raises the possibility of targeting this network to treat the condition, Joutsa said. Electrical brain stimulation is already used to treat patients with various disorders, such as obsessive compulsive disorder, depression, Parkinson's disease and essential tremor. It is also currently being tested for the treatment of additional neurological conditions, such as traumatic brain injuries. 

In theory, brain stimulation may also be able to help prolong the beneficial effects of speech therapy in some patients, Catherine Theys, the study's lead author and an associate professor of psychology at the University of Canterbury in New Zealand, told Live Science. The new findings could help clinicians make more informed decisions about which treatments to select for each patient, she said. 

However, there is a "long road ahead," as it may take years for this vision to be realized, Joutsa said. 

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!

People who carry a rare gene variant are about half as likely to develop Parkinson's disease than people who carry a different version of the gene, a new study finds.

Researchers have started to unravel exactly how this genetic quirk might protect against Parkinson's — by preserving the function of a crucial enzyme needed for cells' metabolism and survival. Someday, a better understanding of the protective mechanism could lead to new treatments for the disease, scientists wrote in the report, published Jan. 3 in the journal Molecular Psychiatry.

"This study advances our understanding of why people might get Parkinson's and how we might develop new therapies for this devastating disease," senior study author Dr. Pinchas Cohen, dean of the University of Southern California (USC) Leonard Davis School of Gerontology, said in a statement.

Parkinson's disease emerges when movement-controlling cells in the brain die off over time. The loss of these neurons causes the well-known movement symptoms of the disease, such as tremors, muscle stiffness and impaired balance, as well as lesser-known symptoms, including emotional changes, sleep disturbances and cognitive decline.

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

Scientists don't yet fully understand what triggers the neuron loss in Parkinson's, but the dysfunction of mitochondria, the powerhouses of cells, has long been considered a hallmark of the disease. The gene variant uncovered in the new study is related to the function of mitochondria, underscoring the importance of this connection.

The majority of our DNA lies tucked away in cells' control centers, or nuclei, but mitochondria actually carry their own set of DNA that's passed down from mother to offspring. In previous research, Cohen and colleagues found that a tiny protein made in the mitochondria, called SHLP2, appears key to the powerhouses' function and declines with age. Later, other researchers found that certain versions of the gene for SHLP2 are tied to a lower Parkinson's risk, but it wasn't clear why.

So Cohen and his collaborators zoomed in on the SHLP2 gene in their latest study. 

First, they screened for different versions of the gene in the mitochondrial DNA of thousands of people who participated in three large, long-term studies: the Health and Retirement Study, the Cardiovascular Health Study, and the Framingham Heart Study. The protective version of SHLP2 appeared in 1% of these individuals, all of whom were of European ancestry, and it was associated with half the chance of Parkinson's disease, compared with other versions of the gene.

Through experiments with human cells in lab dishes and additional tests with mice, the researchers found that the gene variant likely boosts both the stability and the prevalence of the SHLP2 protein. These changes, in turn, prevent dysfunction in a key enzyme in mitochondria, they found.

Together, the researchers' results suggest that a potential treatment strategy for Parkinson's could involve supplying cells with this super stable, protective SHLP2 protein, to help keep their mitochondria working. But this idea will require much more research to confirm.

"Our data highlights the biological effects of a particular gene variant and the potential molecular mechanisms by which this mutation may reduce the risk for Parkinson's disease," first study author Su-Jeong Kim, an adjunct research assistant professor of gerontology at the USC Leonard Davis School, said in the statement.

"These findings may guide the development of therapies and provide a roadmap for understanding other mutations found in mitochondrial microproteins," she said.

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

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!

About 20% to 30% of people carry versions of an immune-related gene that may protect against Alzheimer's and Parkinson's disease, a massive new study across a diverse set of ethnic groups has found.

In the study, people carrying a version of the human leukocyte antigen (HLA) gene known as HLA-DRB1*04, or DR4 for short, had 8% to 15% lower odds of developing these neurodegenerative diseases.

What's more, these individuals harbored fewer of the abnormally folded brain proteins, such as tau tangles, that are hallmarks of these conditions. That hints that the gene variants may protect against such diseases by preventing these proteins from accumulating.

The findings, published Aug. 29 in the journal PNAS, could have implications for the development of novel vaccines against Alzheimer's and Parkinson's.

Related story: Could vaccines prevent and treat Alzheimer's disease?

Alzheimer's and Parkinson's are characterized by the progressive loss of specific neurons, or nerve cells in the brain, and both conditions are linked to a buildup of abnormal proteins. In Alzheimer's, these proteins include so-called tau tangles and amyloid-beta plaques, while in Parkinson's, a protein called alpha-Synuclein misfolds and clumps to form "Lewy bodies." There's also growing evidence that tau tangles play a role in Parkinson's.

And past research suggests that misfiring immune responses may underpin the development of both Parkinson's and Alzheimer's.

Shape-shifting HLA proteins lie at the core of the adaptive immune system, which tailors the body's responses to pathogens, like viruses. In a smaller, past study, study co-author Dr. Emmanuel Mignot, a neuroimmunologist and professor at Stanford University, found that certain variants of a gene called HLA-DRB1, which codes for an HLA protein, were linked to a reduced risk of both Alzheimer's and Parkinson's.

This was striking because the two diseases are so different, Mignot told Live Science. 

To pin down the connection, Mignot and his colleagues looked at a massive collection of genome-wide data from 176,000 people of European, Asian, Latin American and African American ancestry. These individuals had either Alzheimer's or Parkinson's, and their genetics were compared to those of people without the conditions.

They found a strong protective effect for those who carried the DR4 gene variant. Certain subtypes of the variant — specifically HLA-DRB1*04:04 and HLA-DRB1*04:07 — showed the strongest correlation, while HLA-DRB1*04:01 and HLA-DRB1*04:03 had intermediate effects.

To explain how these gene variants may protect against neurodegenerative diseases, the researchers homed in on tau. Studies have shown that abnormal tau proteins are more likely to misfold, aggregate and then spread between cells, causing tau in those cells to misfold too. Mignot and his team hypothesized that an immune response against tau may confer protection from both Alzheimer's and Parkinson's.

In lab experiments, they found that the HLA-DRB1*04:04 and HLA-DRB1*04:01 subtypes bind a tau fragment called PHF6, which is found primarily in Alzheimer's. Specifically, these subtypes latch onto an altered version of PHF6 that's been tied to tao tangles. Binding PHF6 could jumpstart an immune response against the fragment and, in theory, reduce the spread of tau tangles and thus delay the onset and progression of neurodegeneration, the authors hypothesized.

Related: Alzheimer's directly kills brain cells that keep you awake

In further support of this idea, the HLA variants were tied to having fewer tau tangles in the brain, the team found by reviewing data gathered from autopsied brains of people who'd died of Alzheimer's. To a lesser extent, those people also had fewer amyloid beta plaques.

"This is a very interesting study … providing additional evidence of the involvement of the immune system in the pathogenesis of … Alzheimer's and Parkinson's," Wassim Elyaman, a neurologist at Columbia University Irving Medical Center who was not involved in the research, told Live Science in an email.

But although the genetic analysis is strong, the researchers need to do more immune cell- and blood-based studies to pin down how certain versions of tau are connected to Alzheimer's and Parkinson's, Elyaman added. Someday, the innovative study may pave the way for developing novel immunotherapies or vaccines, he said.

Mignot envisions vaccinating people who carry HLA-DRB1*04 with tiny bits of the tau fragment PHF6. This would trigger an immune response against tau and possibly "delay the onset of Alzheimer's and Parkinson's or reduce disease progression, because you would delay the spreading of tau," he explained.

As next steps, Mignot hopes to test that hypothesis in genetically modified mice made to carry the protective HLA gene variant. If it works in mice, it could then be tried in humans.

Sir Ian Wilmut, the scientist who led the cloning of Dolly the sheep, has died at the age of 79.

Wilmut led the University of Edinburgh team that successfully created Dolly, the first mammal to be cloned from an adult cell, in 1996. 

Other researchers had managed to clone mammals by splitting embryos in a test tube and implanting them in adults. But Dolly — named after the singer Dolly Parton — was cloned from the mammary gland of a 6-year-old Dorset Finn ewe and was the first to be grown from an adult somatic (body) cell.

Related: Single bee is making an immortal clone army thanks to a genetic fluke

In 2017, Wilmut revealed that he had been diagnosed with Parkinson's disease.

"We are deeply saddened to hear of the passing of Professor Sir Ian Wilmut. He was a titan of the scientific world," Sir Peter Mathieson, principal and vice-chancellor of the University of Edinburgh, said in a statement. 

Mathieson added that Wilmut's breakthrough "transformed scientific thinking at the time" and "continues to fuel many of the advances that have been made in the field of regenerative medicine that we see today." 

How was Dolly the sheep cloned?

Animals had been cloned from somatic cells before Dolly, notably frogs cloned from skin cells in 1958 by British biologist John Gurdon. But Dolly was significant because decades of failed attempts had made biologists think that the process in mammals was all but impossible.

The scientists made Dolly by extracting DNA from a cell taken from an adult sheep's mammary gland, placing it in an empty sheep egg cell and zapping it with electricity. This transformed the egg into an embryo, which was then implanted inside a surrogate sheep to bring to term.

The breakthrough led to an explosion of research into stem cells and their medical applications.

Following Dolly's July 1996 birth, pigs, deer, rats, bulls, horses and macaques were successfully cloned, and scientists soon began inducing stem cells to grow into a vast array of tissue types — driving stem cell therapy for genetic diseases into the mainstream.

How long did dolly the sheep live?

Dolly died in 2003 after living to age 6, around half the typical 10-to-12-year lifespan of a sheep, and had a number of clone sisters taken from the same batch of cells as her.

"The birth of Dolly and the new understanding of the opportunity to change the functioning of cells made researchers consider other possible ways of modifying cells," Wilmut told Live Science in 2017.

Following his work on Dolly, Wilmut continued to genetically engineer and clone sheep in an effort to make stem cells and create milk with proteins that could treat human diseases.

Wilmut retired in 2012, and received a knighthood in 2008. Following his Parkinson’s diagnosis, he took part in the testing of new types of treatments for the degenerative disease.

In an unusual case, a man's trip to the dentist indirectly triggered bleeding in his brain and led to him being diagnosed with a rare genetic disorder.

Half an hour after having two teeth extracted, the man in Australia, who was in his late 60s, suddenly felt dizzy and started throwing up. His vision was distorted to the point where he saw objects as if they'd been rotated 90 degrees counterclockwise.

Soon after, he went to the emergency department, where doctors determined that he had high blood pressure and his eyes were flickering to the left. He also walked unsteadily and kept falling to the right. A computed tomography (CT) scan revealed that the lower left half of his brain was bleeding — a condition known as intracerebral hemorrhage (ICH). 

ICH is a common form of stroke that can be triggered by many things, including abusing drugs like amphetamine, brain cancer, physical trauma and extremely low temperatures. For example, one woman with a history of high blood pressure developed it after taking part in the "Ice Bucket Challenge." 

Related: This man had a key lodged in his brain. Here's how he survived.

However, prior to the man's unusual case, there'd been only three other reports of people developing ICH after visiting the dentist. In the new case, published Aug. 2 in the journal BMJ Case Reports, doctors believe the man's ICH was likely triggered by a sudden increase in blood pressure following his dental procedure. 

There was, however, one more part of the puzzle to decipher. 

When probing the man's medical history, the doctors found that six weeks before his trip to the dentist, he'd been referred for a CT scan after his general practitioner suspected he had Parkinson's disease, a progressive disease that kills neurons and causes movement issues. At the time, doctors didn't find any issues with the blood vessels in the man's brain, but they did notice signs of white matter disease — a condition in which reduced blood flow causes damage to nerve fibers that pass information between different parts of the brain. The emergency department doctors then confirmed these signs of white matter disease with a magnetic resonance imaging (MRI) scan.

To pinpoint the cause of the white matter disease, the case report authors analyzed the man's DNA and found that he had a mutation in a gene called NOTCH3, which is associated with a rare, inherited disease that causes the walls of blood vessels to thicken, reducing the flow of blood through the brain. This condition is known as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). 

CADASIL is often very difficult to diagnose, given severe cases only affect 2 in every 100,000 people and the disease's common symptoms, such as vision problems, feeling weak and struggling to walk, can often resemble other neurological conditions, such as multiple sclerosis. 

ICH was originally thought to be a rare complication of CADASIL, the case report authors noted. However, recent research suggests it may be a more common complication than previously thought. Whether or not CADASIL and ICH are often linked, the case report authors flagged that this is the first time ICH has been reported in a patient with CADASIL following a dental procedure. 

Following the man's emergency department visit, doctors prescribed him medication to treat his high blood pressure, and three months later, he reported that his symptom of unsteadiness had improved and his vision had returned to normal. He has since been put on a long-term course of aspirin to improve the blood flow in his brain and help prevent further strokes. 

Clumps of proteins found in the brains of people who have Parkinson's disease are also found somewhere else in the body — inside the appendixes of healthy people.

This finding has led researchers to study the link between the appendix and the risk of developing Parkinson's. For example, an October 2018 study found that removing the appendix was associated with a decreased risk of developing the disorder, Live Science reported.

But new findings suggest the opposite — removing the appendix is associated with an increased risk of developing Parkinson's. The study, which has yet to be published in a peer-reviewed journal, will be presented later this month at Digestive Disease Week, a scientific meeting focused on digestive diseases. [3 Myths About Parkinson's Disease]

The new study looked at data on more than 62 million patients, using a database of records from 26 major healthcare systems across the U.S. The researchers identified patients who had appendectomies — surgery to remove the appendix — and flagged those who went on to develop Parkinson's disease at least six months later.

The scientists found that, out of the more than 488,000 patients who had their appendixes removed, 4,470 (0.9%) of them went on to develop Parkinson's disease. Of the remaining 61.7 million patients who didn't have appendectomies, only around 177,000 (0.3%) later developed Parkinson's.

The findings suggest that the risk of developing Parkinson's disease is around three-fold higher for people who had appendectomies than those who did not, regardless of age, gender or race.

However, senior author Dr. Gregory Cooper, a professor of medicine at Case Western Reserve University in Cleveland, said, "at this point it's still an association," and not a cause-and-effect finding. In other words, the study does not prove that having the appendix removed causes Parkinson's.

One possible explanation for the increased risk found in the study is that, during an appendectomy a specific agent – called alpha-synuclein proteins – are released into the body and travel up to the brain, Cooper said. These proteins are known to form clumps called Lewy bodies — a tell-tale sign of Parkinson's disease.

Still, this explanation is "speculative," Cooper told Live Science.

Reverse causality?

Viviane Labrie, an assistant professor of neuroscience at Van Andel Research Institute in Michigan who was not a part of the new research, noted that the study "doesn't have a long follow-up window." That means that the researchers could only link appendectomies to the onset of Parkinson's movement problems, she said.

But these movement problems, or motor symptoms, don't truly represent the onset of the disease, Labrie told Live Science. Rather, Parkinson's disease has a roughly 20 year "prodromal period,"before these tell-tale symptoms appear. During this time, other less-obvious symptoms may occur. 

For example, during the prodromal period, people with Parkinson's may experience symptoms such as constipation or other digestive issues, Labrie said. But, complicating matters further, those symptoms can increase the risk of appendicitis — the inflammatory condition that leads to an appendectomy. So, it's possible that the prodromal symptoms of Parkinson's disease may be causing the appendicitis and the subsequent surgery, and not the appendix removal causing Parkinson's disease, she said.

Labrie was the senior author of a study published in October 2018 in Science Translational Medicine, which used data from a Swedish database of more than 1.6 million people that tracked patients for up to 52 years. That report found that people who had their appendix removed when they were young were 19% to 25% less likely to develop Parkinson's later in life.

The "key difference between [the Swedish] study and the [new] US study is [the] length of time the patients were followed," Labrie said.

Cooper agreed that a limitation of his study involved the limited data available during the follow-up period. This is because the patient information was de-identified, so the researchers couldn't see how long it took for specific patients to develop Parkinson's after an appendectomy. But because the database has been gathering data since 1997, at least some of the patients were followed for nearly 30 years, he said.

In addition, the researchers didn't have access to patient medical records, so they couldn't look at other factors that may have influenced the results, such as specific symptoms or medications, Cooper added.

The risk is still really low

Ultimately, there still isn't a consensus on if appendectomies are associated with a higher risk of Parkinson's disease.

A 2016 study published in the journal Movement Disorders found similar results to this new study — that an appendectomy was associated with an increased risk of Parkinson's disease risk 10 or more years after the surgery; but that risk was much smaller than that noted in the recent study. Other research, such as a 2018 paper published in Movement Disorders, found little to no association between appendectomies and Parkinson's disease.

In any case, Cooper stressed that while the study did find an association between an appendectomy and the risk of developing Parkinson's disease, the risk is very low: Less than 1% of people who developed Parkinson's disease had undergone an appendectomy, he said.

"I don't want people to come out of here and say, 'Well, I have appendicitis I'm not going to get my appendix taken out because I don't want to get Parkinson's disease'," he said. "If you have appendicitis … you should get your appendix out."

This was reminiscent of what Labrie told Live Science last fall, when her paper was published: "One of the things that we don't want to get across to people is that [they] should be having preventative appendectomies or that just because you have an appendix, you're going to get Parkinson's disease."

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Originally published on Live Science.

Parkinson's is a neurodegenerative disease that primarily affects the part of the brain responsible for normal movement. A neurodegenerative disease is one that attacks the cells of the central nervous system to the point where they either stop working properly or die altogether. Such disorders generally get progressively worse over time.

The condition is named after James Parkinson who, in his 1817 work "An Essay on the Shaking Palsy",  wrote a detailed account of what he referred to as shaking palsy (paralysis agitans). The condition was eventually re-branded Parkinson's by Jean-Martin Charcot, a French neurologist.

"Parkinson's is the most common neurodegenerative movement disorder," said Dario Alessi, a professor of signal transduction and director of the Medical Research Council Protein Phosphorylation and Ubiquitylation Unit at the University of Dundee in Scotland.

Around 500,000 people in the United States are currently diagnosed as having Parkinson's, though according to the National Institute of Neurological Disorders and Stroke (NINDS), as many as one million people could have it. Globally, as many as 10 million people are thought to have Parkinson's, according to the charity Parkinson's Europe. 

What are the symptoms of Parkinson's disease?

The main motor symptoms of Parkinson's include tremors and involuntary shaking, bradykinesia (slowness of movement), rigidity, muscle stiffness and gait disturbances, including balance problems, Alessi told Live Science. This is because the primary characteristic of idiopathic Parkinson's disease is that the brain cells in the midbrain that produce dopamine, the chemical that coordinates movement, start to die.

"Other symptoms may include sleep issues, constipation, mood problems, anxiousness and reduced smell," he said. 

What causes Parkinson's Disease?

The definitive cause of Parkinson's is not yet known. This is why it is called idiopathic — arises spontaneously — Alessi said. 

"The general belief is that genetic and environmental factors, as well as advancing age, play a role," he said. "In some individuals, changes in several genes are associated with the development of Parkinson's. One example is the LRRK2 genes. As such, individuals carrying certain genetic changes are more likely to develop Parkinson's disease. Curiously, men are 1.5 times more likely than women to develop the condition."

According to Parkinson's Europe, the vast majority of people who are diagnosed with Parkinson's are over the age of 60, though one in 10 is under 50.

Besides age and sex, other risk factors for Parkinson's disease include:

• Heredity: Some genetic mutations may contribute to the development of Parkinson's and can slightly increase a person's risk. But most cases of the disease are not caused by inheriting genes linked to it. Only about 10 percent of people with Parkinson's are genetically predisposed to the condition, according to the American Parkinson Disease Association.
• Exposure to toxins: Studies have shown that environmental factors — such as exposure to pesticides, herbicides (like Agent Orange) and drinking well water — may be tied to an increased risk of Parkinson's, but that risk is relatively small.
• Repeated head injuries: When these injuries trigger a loss of consciousness, they have been linked with an increased risk of Parkinson's.

How is Parkinson's disease diagnosed?

There is no specific test, such as a blood test or MRI, that can be used to diagnose Parkinson's. Instead, the diagnosis is based on a constellation of findings from a thorough examination, said Dr. Danny Bega, a neurologist at Northwestern University Feinberg School of Medicine in Chicago.

Parkinson's shares similarities with a number of other diseases and disorders.

"There are atypical Parkinsonian syndromes including multiple system atrophy, Lewy body dementia and progressive supranuclear palsy that can initially look very much like Parkinson's, but eventually take a different trajectory in terms of rate of progression, additional clinical symptomatology, responsiveness to symptomatic therapies, and potentially underlying neuropathology," Alessi said.

Parkinson's typically develops slowly over time, making it hard to detect in the early stages of the disease. In addition, the progression of symptoms and their intensity can vary from one person to another. 

Diagnosis may partially come from identifying symptoms during a physical exam, such as stiffness and slow movement, Bega said. Because this disease can be tricky to diagnose, it's best for patients to work with a neurologist or movement-disorder specialist who sees these problems daily, he said.

Can you treat Parkinson's disease?

Many medications are available to treat the symptoms of Parkinson's disease, but none of them can slow the disease's progression, said Bega.

There are a number of different medications that can help with alleviating motor symptoms as well as non-motor symptoms. In general, the most effective treatment for motor symptoms is dopamine cell replacement transplantation, which involves "injecting new dopamine producing neurons into the part of the brain to replace the dead or dying neurons," according to the Cure Parkinson's Trust. 

"Many patients initially have a good response to medication but, as the disease progresses, symptoms become more complex and may have more of an impact on someone's daily life," Alessi said. "We are now better at managing the advanced stages of Parkinson's, but this does not take away from the fact that we need interventions that slow or stop the progression of the disease."

Studies have suggested that being physically active may slow the progression of Parkinson's symptoms. Bega said he encourages regular exercise — stationary biking, swimming, strength training or doing tai chi — to improve mobility, balance and mood for people with the disease.

Knowledge around the underlying biology of Parkinson's has increased exponentially in recent years. 

"There are some very exciting new targets that are being explored in the clinic," Alessi said.

Parkinson's research involves the protein alpha-synuclein. In autopsies, many brain cells of people who'd had Parkinson's disease have been found to contain Lewy bodies, which are unusual clumps of alpha-synuclein.

These clumps of protein in the brain are the pathological hallmark for Parkinson's and may be one reason the brain is not working properly in those with the condition, Bega said. If researchers can prevent the protein from clumping into Lewy bodies, by either clearing them out or stopping their spread within brain cells, then that may lead to a method of stopping the disease's progression, said the Michael J. Fox Foundation for Parkinson's Research.

Such treatment could ultimately slow — or even halt entirely — Parkinson's. "Our hope is that in the next five to 10 years the first medications are approved that, for the first time, will slow the progress of Parkinson's," Alessi said. "This would represent a landmark in medicine if it could be achieved."

Additional resources:

• Learn more about Parkinson's disease from the Mayo Clinic.
• Read what the National Institute of Aging has to say about Parkinson's disease.
• Learn more about research on Lewy bodies from the National Institute on Aging.

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

Amphetamines are central nervous system (CNS) stimulants, also called psycho-stimulants, that are often used to treat attention deficit hyperactivity disorder (ADD and ADHD), narcolepsy, Parkinson's disease and obesity, according to the Center for Substance Abuse Research (CESAR) at the University of Maryland. Because of their high potential for abuse, the substances are also classified as Schedule II drugs by the U.S. Drug Enforcement Administration (DEA).

Amphetamines are derived from ephedra (Ephedra sinica), a plant native to China and Mongolia. For centuries, many cultures have used ephedra as a stimulant and for treating congestion and asthma, according to the National Center for Complementary and Integrative Health (NCCIH). The plant contains ephedrine and pseudoephedrine, which are natural alkaloids, or nitrogenous organic compounds that cause a physiological response in humans. These chemicals are the basis on which amphetamines (including methamphetamine) were created.

The history of amphetamine

Nagai Nagayoshi, a Japanese chemist and pharmacologist, first isolated ephedrine in 1885. Only two years later, in 1887, Lazar Edeleanu, a Romanian chemist, synthesized amphetamine from ephedrine, according to the University of Arizona's Methamphetamine and Other Illicit Drug Education (MethOIDE) program.

In 1929, Gordon Alles, a U.S. biochemist, discovered that amphetamine had physiological effects. Soon after Alles' discovery, pharmaceutical companies developed amphetamine medications for treating congestion and asthma, according to a review published in the American Journal of Public Health in 2008. From 1933 to 1948, amphetamine was included in an over-the-counter nasal-congestion inhaler called Benzedrine.

Additional clinical trials found that amphetamine had positive effects on weight loss, narcolepsy and depression. It's popularity then grew during World War II as active service members from the U.S., Japan, Germany and England were administered the drug to treat mild depression and to enhance alertness and endurance.

Amphetamines have been used since then in the development of a variety of drugs, most notably Adderall and Ritalin, which treat ADD and ADHD. Addiction to amphetamines has been an issue since the 1940s, but it escalated in the 1980s with increased illicit production of methamphetamine, a very addictive stimulant known for its euphoric effects.

How amphetamines work

Amphetamines are used in treatments for ADD and ADHD, obesity, narcolepsy, and Parkinson's disease, according to CESAR.

"People with ADHD [are hypothesized to] have too little dopamine in the prefrontal cortex — the rational thinking, cognitive, planning part of your brain — the part of your brain that tells the rest of your brain to calm down," said Catherine Franssen, assistant professor of biopsychology and director of neurostudies at Longwood University in Virginia.

An amphetamine-based medication, such as Adderall or Ritalin, increases dopamine production in the connections between the prefrontal cortex and other locations in the brain, Franssen explained. This allows the prefrontal cortex to regain control.

Certain formulations of amphetamine, typically pseudoephedrine, are used in medications that treat cold symptoms, such as Sudafed, Franssen said. The amphetamine stimulants reduce the swelling of the blood vessels in the nose; this helps open up the airways, allowing for easier breathing. The medications are available without a prescription but are stored behind the pharmacy counter because they can be illegally used to brew methamphetamine, according to the American Council on Science and Health.

There's some evidence that amphetamines may treat obesity by acting as appetite suppressants. A 2015 clinical trial published in the journal Frontiers in Endocrinology reported that patients who took amphetamine medications experienced increased weight loss and motivation. The mechanism was unclear, and more research is needed to determine if amphetamines can be used for long-term weight loss and maintenance.

Amphetamine side effects

When taken properly, amphetamine-based medications can be safe and effective. But as with any prescribed medication, there are potential side effects.

Amphetamines can have a powerful effect on the body and brain, even when taken only once. According to MedlinePlus, side effects of taking amphetamines include:

• Enhanced mood
• Increased wakefulness and physical activity
• Increased respiration
• Insomnia
• Increased heart rate and blood pressure
• Irregular or rapid heartbeat
• Cardiovascular collapse
• Reduced appetite
• Changes in sex drive
• Hyperthermia
• Permanent brain damage
• Memory loss, confusion, paranoia and hallucinations
• Convulsions or Parkinson's-like tremors
• Cardiovascular collapse or stroke

Side effects such as enhanced mood are linked to the increase production and release of dopamine, a neurotransmitter associated with pleasure.

Amphetamines also cause an increase in norepinephrine, the hormone involved with the activation of the sympathetic nervous system, which is what controls our "fight-or-flight" mechanism, Franssen said. Norepinephrine causes the physical side effects, such as increased respiration, heart rate and blood pressure.

Together, those two chemicals can also have other mental effects.

"The increase of dopamine, as well as the activation of the sympathetic nervous system, [can lead to] hallucinations and psychosis, similar to schizophrenia," Franssen said.

Addiction and abuse

Amphetamines, particularly methamphetamine, can be highly addictive.

Amphetamine can cause the brain to produce such high amounts of dopamine that the brain compensates by getting rid of dopamine receptors, Franssen said, similar to how we cover our ears to decrease the volume when someone is shouting at us. 

Removing these receptors decreases the person's ability to feel pleasure and can increase depression or suicidal thoughts when the person's not using the drug, according to American Addiction Centers. Those depressing feelings may drive people to continue using the drug so that the dopamine and the positive feelings it produces return.

In 1971, the Bureau of Narcotics and Dangerous Drugs — now the U.S. DEA — classified all forms of amphetamine, including the highly addictive methamphetamine, as Schedule II drugs. The classification means the drugs have an accepted medical use but also a high potential for abuse.

Beginning in the 1980s, abuse of amphetamine skyrocketed as illegal methamphetamine production took off. This period also saw a surge in prescriptions of amphetamine drugs for treating attention deficit disorders. Abuse and medical use of amphetamines has continued to increase over the past decade.

It wasn't until 2004, according to the NCCIH, that the U.S Food and Drug Administration banned the sale of any supplement containing ephedrine, which had become a common supplement for athletes. The ban stemmed from a rise in the number of health issues related to the drug and several deaths of people looking to increase endurance and lose weight with ephedrine supplements, according to Harvard Health Publishing.

In the U.S., an estimated 4.8 million people ages 12 and up abused their amphetamine-based prescriptions and about 1.7 million used methamphetamine in 2015, according to a National Survey on Drug Use and Health. However, it's difficult to accurately track methamphetamine use, because the drug is manufactured and distributed illegally. Additionally, the majority of methamphetamines come from outside the U.S., where they are produced cheaply and illegally with little consequence.

In early 2018, The New York Times reported that methamphetamine use in the U.S. had greatly increased over the past decade. In Portland, Oregon, more than 200 people died from methamphetamine use in 2016; that was three times more than just 10 years earlier, the Times reported. Portland was just one such example of a location that inundated by methamphetamine use.

While the physical changes amphetamines cause in the brain are permanent, several therapeutic treatment programs that can help people overcome their addiction. The most-successful treatments include addiction education, family counseling, cognitive behavior therapy and peer-support groups.

Further reading:

• More about methamphetamine from the National Institute on Drug Abuse.
• Amphetamine, past and present.
• Fact sheet on amphetamine from the U.S. DEA.

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

A new experimental therapy for Parkinson's disease that involves injecting millions of special stem cells into the brain of patients with the condition is currently being tested in a clinical trial.

The study, which began in October, is conducted by researchers at Kyoto University in Japan. So far, researchers have started to treat one man in his 50s, according to AFP.

Although previous studies have tested stem cell therapies for Parkinson's, the new study is the first to use so-called induced pluripotent stem cells, or iPSCs. These are "adult" cells (like blood or skin cells, as opposed to embryonic cells) that have been reprogrammed so that they resemble cells in early development, and they have the potential to form any cell type in the body.

For the study, the researchers used iPSCs to create "dopaminergic progenitor" cells, or the cells that give rise to brain cells that produce dopamine, a brain chemical that is needed to control muscle movement. In Parkinson's disease patients, the brain cells that produce dopamine die off, leading to symptoms such as tremors and difficulty with walking, movement and coordination.  [10 Things You Didn't Know About the Brain]

In the new trial, the researchers hope to show that these transplanted stem cells will help replace the lost dopamine-producing cells and restore dopamine production, according to The Michael J. Fox Foundation.

For the treatment, the researchers injected 2.4 million stem cells into the left side of the man's brain, in an operation that took 3 hours, according to AFP. The patient will now be monitored for side effects, and if no problems occur, the researchers will inject another 2.4 million stem cells into the right side of his brain.

The researchers plan to enroll a total of seven patients in the trial and to track the patients for two years.

The iPSCs were derived from donors, so the patients will need to take drugs to suppress their immune system to prevent rejection of the transplanted cells, according to Kyoto University.

Originally published on Live Science.

Having a single concussion may increase a person's risk for Parkinson's disease, a new study suggests — but the overall risk of developing the disease still remains low.

The study, which analyzed information from more than 320,000 U.S. veterans, found that those who'd experienced a mild traumatic brain injury (TBI), often called a concussion, were 56 percent more likely to be diagnosed with Parkinson's than those who'd never had a concussion.

Although the study participants had served in the military, their concussions were often reported to have happened during their civilian lives, said senior study author Dr. Kristine Yaffe, a professor of psychiatry, neurology and epidemiology at the University of California, San Francisco (UCSF) School of Medicine. "As such, we believe [the study] has important implications for the general population," Yaffe said in a statement.

Previous research has found a link between Parkinson's disease and moderate to severe TBIs; however, this is the first large study to show a link between milder head injuries and Parkinson's, the researchers said. [10 Things You Didn't Know About the Brain]

However, it's important to note that, even if participants experienced a concussion, their risk of Parkinson's was still very low. Overall, 360 out of 76,297 participants with a concussion, or 0.47 percent, developed Parkinson's; and 543 out of 72,592 participants with moderate to severe TBIs, or 0.75 percent, developed the disease.

Why is there a link?

The researchers analyzed health information from 325,870 veterans, ages 31 to 65, using three U.S. databases from the Veterans Health Administration. About half of the participants had been diagnosed with either a concussion or a more serious moderate to severe TBI at some point in their lives. (The study was not able to look at the frequency of TBI, so some particpants may have experienced more than one TBI.) Participants were then followed for an average of 4.6 years.

During the follow-up time, 1,462 participants were diagnosed with Parkinson's. Of these, 949 participants with any TBI, or 0.58 percent, developed the disease, compared with 513 participants with no TBI, or 0.31 percent.

The risk of Parkinson's was higher for those who'd had a moderate to severe TBI. These participants were 83 percent more likely to develop the condition than those who'd never had a TBI.

It's not clear exactly why head injuries are linked with an increased risk of Parkinson's. But generally, head injuries can cause inflammation in the brain, which may lead to changes in cells and brain structures that contribute to Parkinson's, Dr. Barbara Changizi, a neurologist at The Ohio State University Wexner Medical Center, told Live Science in a 2016 interview. A person's genetics may play a role as well, Changizi said.

Some studies have also found abnormal brain deposits of a protein called alpha-synuclein, which is a hallmark of Parkinson's, in people with traumatic brain injuries, the authors of the new study said.

The study "highlights the importance of concussion prevention, long-term follow-up of those with concussion, and the need for future studies" to investigate the mechanisms behind the link, as well as factors that might reduce the risk of Parkinson's after a concussion, said lead study author Dr. Raquel Gardner, an assistant professor of neurology at the UCSF School of Medicine.

The study was published April 18 in the journal Neurology.

Original article on Live Science.

In an effort to find new treatments for Parkinson's disease, researchers are sending their experiments to space.

This Monday (Aug. 14), researchers will launch a key Parkinson's disease protein, called LRRK2, to the International Space Station (ISS). The microgravity conditions in space should offer a better test environment for their experiments with this protein, the researchers said.

The materials for their experiments will travel aboard the SpaceX Dragon capsule as part of a mission to send supplies and science experiments to the ISS.

The work is a collaboration between The Michael J. Fox Foundation for Parkinson's Research and the Center for the Advancement of Science in Space (CASIS).

LRRK2 is a type of protein that modifies other proteins. Mutations in the gene that codes for LRRK2 are thought to cause Parkinson's disease in some people. Researchers have hypothesized that developing drugs to inhibit LRRK2, or block its activity, could help prevent Parkinson's or slow its progression. [10 Celebrities with Chronic Illnesses]

But before scientists can develop a drug to inhibit LRRK2, they need to know the precise structure of this protein. One way to get a detailed view of its structure is by growing crystals of LRRK2 in lab dishes. However, on Earth, gravity can interfere with the growth of these crystals, and keep them small.

"The quality of our crystals is just not good enough [on Earth]," Sebastian Mathea, a researcher at the University of Oxford who is involved in the LRRK2 project, said during a news conference about the project Tuesday (Aug. 8).

This is where the ISS research comes in: Researchers hope that the microgravity conditions in space will allow the crystals to grow bigger with fewer defects. The scientists can then get a sharper view of the crystal structure.

Scientists will grow the LRRK2 crystals for about a month in space. Then, the crystals will be sent back to Earth, where they will be analyzed with high-energy X-rays, Mathea said.

Parkinson's disease is a progressive neurological disorder that affects people's movement abilities, and can result in symptoms such as tremors, slowed movements and muscle stiffness. There are currently no treatments to stop or reverse the progression of the disease, according to The Michael J. Fox Foundation.

Original article on Live Science.

Parkinson's disease, which involves the malfunction and death of nerve cells in the brain, may originate in the gut, new research suggests, adding to a growing body of evidence supporting the idea.

The new study shows that a protein in nerve cells that becomes corrupted and then forms clumps in the brains of people with Parkinson's can also be found in cells that line the small intestine. The research was done in both mice and human cells.

The finding supports the idea that this protein first becomes altered in the gut and then travels to the brain, where it causes the symptoms of Parkinson's disease.

Parkinson's disease is a progressive movement disorder, affecting as many as 1 million people in the United States and 7 million to 10 million people worldwide, according to the Parkinson's Disease Foundation.

The protein, called alpha-synuclein, is abundant in the brain. And in healthy nerve cells, it dissolves in the fluid within the cell. But in Parkinson's patients, alpha-synuclein folds abnormally. The misfolded protein can then spread through the nervous system to the brain as a prion, or infectious protein. In the brain, the misfolded protein molecules stick to each other and clump up, damaging neurons. [6 Foods That Are Good for Your Brain]

In 2005, researchers reported that people with Parkinson's disease who had these clumps in their brains also had the clumps in their guts. Other research published this year looked at people who had ulcers and who underwent a surgery that removed the base of the vagus nerve, which connects the brain stem to the abdomen. These patients had a 40 percent lower risk of developing Parkinson's later in life compared with people who didn't have their vagus nerve removed.

Both findings suggested the prion may originate in the gut.

But one puzzle remained: how the proteins that became altered in the gut could spread to the brain. The protein had been found in the lumen, or the space inside the gastrointestinal tract, but "nerves are not open to the lumen," said gastroenterologist Dr. Rodger Liddle, senior author of the new paper, appearing today (June 15) in the journal JCI Insight, and professor of medicine at Duke University in North Carolina.  

A key clue to how the protein may move from the lumen into nerve cells came in 2015. Liddle's team discovered cells in the lining of the small intestine that "acted a lot like nerve cells," Liddle said. The cells were endocrine cells, meaning they produce hormones, but they contained neurotransmitters and other proteins normally found in neurons. These cells even appeared to branch out in a similar way that neurons do, to communicate.

When placed near neurons, these endocrine cells behaved a lot like neurons – the endocrine cells moved toward the neurons, and fibers sprouted between the cells, connecting them, Liddle said. The process was captured in a time-lapse video featured in the 2015 study in the Journal of Clinical Investigation.

"It was only afterwards that we started putting these things together — these cells have a lot of nerve-like properties, [so] let's see if they also contain alpha-synuclein. And if they do, maybe they could be the source of Parkinson's disease," Liddle told Live Science. [10 Things You Didn't Know About the Brain]

Now that Liddle's team has shown that the endocrine cells do, in fact, contain the alpha-synuclein protein, the researchers want to establish that the endocrine cells of Parkinson's patients carry the malformed version of the protein, Liddle said.

If they can establish that, Liddle said, they can envision how the corrupted proteins causing Parkinson's disease could spread from the gut lining to the brain, possibly via the vagus nerve.

Previous research has shown that people exposed to certain pesticides and bacteria are more likely to get Parkinson's. Liddle said that one possibility is that these agents may affect the nerve-like endocrine cells in the gut, altering the structure of the alpha-synuclein protein inside the gut cells.

"Maybe it's bacteria, maybe a toxin that people ingest. Maybe they affect the endocrine cell and that corrupts the alpha-synuclein protein, and that spreads from the cell to the vagus nerve to the brain," Liddle told Live Science.

For now, many "maybe's" remain. But if further research supports the hypothesis, it could point the way to new ways to diagnose Parkinson's disease early on, as well as to new approaches to treatment, Liddle said.

"It's possible that if it starts in the gut, then you could create treatments that prevent abnormal alpha-synuclein formation in these cells," Liddle said. "It's possible you could develop dietary ways of treating those cells because those cells are lining the intestine. At this point, it's difficult to imagine, but we will see."

Originally published on Live Science.

A treatment called "deep-brain stimulation" that is used for people with disorders such as Parkinson's disease doesn't have to physically dig into the brain, it turns out. Instead of using invasive methods to electrically stimulate brain cells, a new technique places electrodes on the head to stimulate the brain noninvasively, according to a new study.

Scientists revealed that they could get a mouse to wiggle its ears, paws and whiskers using this new method, they added.

Current techniques for using deep-brain stimulation on human patients involve surgically implanting electrodes deep into the brain, and then using them to send electrical impulses. Doctors usually reserve this invasive therapy for people with severe conditions, such as those with epilepsy whose seizures have not improved with any other treatments. [10 Things You Didn't Know About the Brain]

"Deep-brain stimulation is very useful for helping a lot of people, but it does require surgery," said study senior author Ed Boyden, co-director of the Massachusetts Institute of Technology's Center for Neurobiological Engineering.

A number of noninvasive methods can stimulate cells near the surface of the brain using electrical or magnetic pulses, but these techniques struggle to stimulate deeper regions that doctors might want to reach for therapies.

Now, Boyden and his colleagues have developed a new way to perform noninvasive deep-brain stimulation on mice, raising the possibility that it could work on humans someday.

The new technique is called temporal interference (TI) stimulation. It works by placing electrodes on the head that emit two or more high-frequency electrical signals to a target deep within the brain.

Neurons generally react only to low-frequency electric signals. As such, high-frequency signals will pass through most neurons without effect, the researchers said.

However, when these high-frequency signals meet at the target, they interfere with one another. The spot where they interact will instead experience a low-frequency signal that excites the neurons, the researchers explained.

In experiments on living mice, the researchers confirmed that these electrical signals stimulated targets deep inside the brain and not overlying regions. They could use their technique to alternate between moving a mouse's right paw, whiskers and ears, and then its left paw, whiskers and ears.

The scientists also ran a number of safety experiments to confirm that their new technique did not damage brain tissues. They found that it did not harm neurons, trigger seizures or heat brain cells beyond the natural range of temperature variations seen in the brain. [6 Foods That Are Good For Your Brain]

"If we can figure out a way to stimulate the human brain without surgery, this could not only lead to clinical applications for epilepsy, Parkinson's, depression and other diseases, but you could carry out advanced neuroscience experiments on human volunteers to perturb brain circuits very precisely and learn more about the human condition," Boyden said.

It remains uncertain what challenges this new technique might face before it's used on humans, who have thicker skulls and larger brains. The researchers plan to scale it up to human volunteers soon.

The scientists detailed their findings June 1 in the journal Cell.

Original article on Live Science.

Where do dreams come from? Researchers now say they know: A specific group of cells in the brain stem is responsible for controlling dreaming sleep, also called Rapid Eye Movement (REM) sleep, a new study says.

The study also showed that damage to those cells could lead to a sleeping disorder called REM Behavior Disorder (RBD), which makes a person act out violent dreams.

The findings have far broader implications than pinpointing the neurological source of dreams, though, said the study's principal investigator, John Peever, a professor of cell and systems biology at the University of Toronto. Because previous studies have shown that 80 percent of people with RBD develop incurable brain diseases, the new research could give drug companies a specific group of cells to target for therapies that slow the progression of neurodegenerative diseases. [7 Mind-Bending Facts About Dreams]

"For some reason, the cells in the REM sleep area are the first to be sickened, and then the neurodegenerative disease spreads up into the brain and affects the other areas that cause disorders like Parkinson's disease," Peever told Live Science.

Peever presented his team's results May 29 at the 2017 Canadian Neuroscience Meeting in Montreal. The findings have not been published in a peer-reviewed medical journal.

During a healthy night's sleep, a person cycles through light sleep, deep sleep and REM sleep several times. During REM sleep, the neurons in the brain stem send signals to the brain's cerebral cortex — perhaps drawing the details for the dream from the parts of the brain responsible for learning, thinking and moving — as well as to the body's spinal cord, to prevent muscles from moving, Peever said.

During healthy REM sleep, most people do not move around much, although some do twitch or talk. And although some people are known to walk in their sleep, sleepwalking is not a part of REM sleep, but a part of the deep-sleep cycle, when dreaming doesn't occur.

In contrast, people who have RBD frequently have violent dreams and act them out during their REM sleep, injuring themselves and anyone who might be sleeping next them. 

The disorder was first described by Dr. Mark Mahowald and Dr. Carlos Schenck, of the University of Minnesota. In their book, "In Principles and Practice of Sleep Medicine," published in 1985, the two doctors presented case histories of people with the disorder, including a 77-year-old minister, who behaved violently in his sleep, sometimes injuring his wife; a 60-year-old surgeon, who reported the feeling of being attacked, and who would jump out of bed during nightmares; and a 57-year old retired school principal, who mistakenly punched and kicked his wife while having nightmares.

Peever said that studies done since then have showed that the vast majority of people who have RBD develop one of three progressive brain diseases. One is Parkinson's disease, which is a degenerative disorder of the central nervous system that afflicts the motor system. The second is dementia with Lewy bodies, which causes forgetfulness, fluctuations in alertness, visual hallucinations and trouble walking. The third is a disorder called multiple system atrophy, which affects the part of the nervous system that controls voluntary movement as well as involuntary movements, including blood pressure and digestion.

"REM Behavior Disorder is in fact the best-known predictor of the onset of Parkinson's disease," Peever said. [5 Surprising Sleep Discoveries]

The brain diseases like Parkinson's and dementia with Lewy bodies typically occur six to 15 years after a RBD diagnosis.

Until now, the link between RBD and these neurological diseases has been anecdotal, though, Peever said. Researchers who studied the brains of cadavers from people who suffered from both RBD and a brain disease found damage to the neurons in the brain stem. But that didn't mean the damage had caused RBD.

"There was a correlation, but no causality," Peever said. "What our study has done is taken away the correlation and show causality."

In the new study, Peever and his colleagues first identified which cells were responsible for healthy REM sleep. They used mice with cells in the brain stem that had been genetically modified to be sensitive to light. When they shined a light onto these cells, it activated the REM sleep in the mice. When they deactivated those cells, the mice did not have REM sleep.

Once the researchers had the cluster of neurons pinpointed, they used a genetically engineered virus to deliver a disease-causing protein – the same one that causes Parkinson's disease — into the REM-generating brain cells. The protein caused the cells to become sick and the mice started to exhibit behaviors indicative of people with REM Behavior Disorder, moving around much more during REM sleep.

"We're saying REM sleep cells get sick, and then you develop REM sleep behavior disorder," Peever said.

The long-term strategy of this research is to develop a drug therapy that could treat patients who have been diagnosed with RBD. Such a therapy would likely not cure the patient of RBD, since the brain cells that cause that disorder would have already been damaged, but it could prevent the disease from spreading to the rest of the brain, Peever said.

"You may have RBD, which is still unfortunate, but you won't develop one of those other brain disorders, which are far more disabling," he said.

Originally published on Live Science.

Your brain may start aging at a dramatically faster rate when you hit age 65 — or it may not, depending on which version of a particular gene you have, a new study suggests.

In the study, scientists identified a gene that appears to control the speed at which the brain ages, and they say that a particular version of it may offer protection against a host of age-related neurological diseases, including dementia. [7 Ways the Mind and Body Change With Age]

The gene, called TMEM106B, kicks into action at about age 65. Soon after that, people with bad copies of this gene will have a brain that looks 10 to 12 years older than people of the same age who have working copies, the scientists said.

The discovery may allow doctors to identify which people are at an increased risk for neurological diseases by virtue of having a faulty TMEM106B gene. It also may help develop drugs that target this gene to promote healthier brain aging, the researchers said. The study describing this work appears today (March 15) in the journal Cell Systems.

In recent years, scientists have identified numerous genes associated with Alzheimer's disease, Parkinson's disease and other neurological conditions.

"But those genes explain only a small part of these diseases," said study co-leader Herve Rhinn, an assistant professor of pathology and cell biology in the Taub Institute for Alzheimer's Disease and the Aging Brain at Columbia University Medical Center in New York. "By far, the major risk factor for neurodegenerative disease is aging. Something changes in the brain as you age that makes you more susceptible to brain disease."

The genetic-based instructions expressed by TMEM106B may be that "something," Rhinn said. The instructions may either protect against or accelerate the ravages of aging. [6 Big Mysteries of Alzheimer's Disease]

"If you look at a group of seniors, some will look older than their peers, and some will look younger," said Dr. Asa Abeliovich, a professor of pathology and neurology at the Taub Institute and a co-author of the study. "The same differences in aging can be seen in the frontal cortex, the brain region responsible for higher mental processes."

Previous studies have associated TMEM106B with a rare form of dementia called frontotemporal lobar degeneration. However, the new study shows that the TMEM106B gene is more broadly associated with brain age, and underlies how well seniors maintain their cognitive abilities, according to Rhinn and Abeliovich.

To determine what might control brain aging, the two researchers analyzed genetic data from more than 1,200 autopsied human brains from people who had not been diagnosed with a neurodegenerative disease while alive. They focused on a few hundred genes whose levels of expression had previously been found to either increase or decrease with aging. From this information, they compiled a chart of what they called "differential aging" denoting the difference between someone's true or chronological brain age compared with an apparent brain age.

One gene, TMEM106B, popped out of the data as a genetic driver of differential aging. TMEM106B appears to control inflammation and neuronal loss in the brain. There are two forms of the gene, or alleles: One form is associated with an increased rate, or risk, of brain aging, and the other allele is protective and is thought to prevent such an acceleration of aging.

Everyone has two copies of the gene, and in the general population, about 30 percent of people have two risk alleles; about 50 have one risk allele and one protective allele; and 20 percent have two protective alleles, Rhinn said. [6 Foods That Are Good For Your Brain]

"From what we could see, the effect of the [TMEM106B] risk allele is additive, in the sense that the brain of elderly people with two copies of the risk allele 'looks' five years older than the [brain] of people with only one copy of risk allele, and [they] themselves 'look' five years older than people with no risk allele," Rhinn told Live Science. "It is indeed one of our hypotheses that TMEM106B regulates systematic response to age-associated stressors in [the] human brain."

In the same study, Rhinn and Abeliovich also looked at the brains of people who had been affected by Alzheimer's disease and/or Huntington's disease during their lives, and they observed the same effect of TMEM106B on brain aging in those people.

"TMEM106B begins to exert its effect once people reach age 65," Abeliovich said. "Until then, everybody's in the same boat, and then there's some yet-to-be-defined stress that kicks in. If you have two good copies of the gene, you respond well to that stress. If you have two bad copies, your brain ages quickly."

TMEM106B may be an attractive target for researchers hoping to create treatments that could slow down brain aging, although such therapies would take many years to develop, the researchers 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.

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.

As we get older, our brain cells show changes, and now a new study finds that certain changes happen so reliably that by themselves they can reveal a person's age.

In the study, researchers analyzed brain tissue samples from 480 people who died between the ages 16 and 106. None of these individuals had experienced a brain disease before their death.

The researchers then examined whether they could find differences between the older brains and the younger ones by looking at the level of their expression of certain genes, meaning which genes were "turned on" and "turned off."

They found that, with age, certain types of brain cells called glial cells showed a shift in their gene expression patterns in certain regions of the brain. In contrast, no such change was seen in the brain's neurons, which are the "signaling cells" of the brain. Glial cells provide support for neurons.

What's more, when the researchers looked at whether the gene expression pattern inside the different types of cells could be used to predict a person's age, they found that the gene expression levels of glial cells were most strongly linked with a person's age. [7 Ways the Mind and Body Change With Age]

"These findings reinforce a growing body of evidence implicating [glial cells] in aging," the researchers, from the University College London, wrote in yesterday's (Jan. 10) issue of the journal Cell Reports.

Some of the biggest shifts in glial-cell gene expression were seen in the hippocampus (which is involved in memory) and the substantia nigra (which is involved in movement).

Because these two brain areas are also affected in people in the early stages of Alzheimer's disease and Parkinson's disease, the study may provide insights into the roles that glial cells may play in these age-related diseases, the researchers said.

"We believe that our data, and computational approaches, provide a powerful resource for further study of the cellular and molecular changes taking place during human brain aging, and provide insights into the pre-clinical cellular phase of dementia," the researchers said.

Still, more research is needed to better understand the cellular changes seen in the study, and how glial cells and neurons interact during aging in general and in people with age-related diseases, they said.

Original article on Live Science.

Former U.S. Attorney General Janet Reno has died at age 78 from complications of Parkinson's disease, her family announced today. But how do people die from this disease?

In patients with Parkinson's disease, the brain cells that produce a chemical called dopamine start to die off. It's not clear what triggers the death of these cells, but researchers do know that dopamine is important for the control of muscle movement. Parkinson's patients experience symptoms such as tremors, slowed movements, muscle stiffness and impaired balance.

Parkinson's itself is usually not considered a deadly disease, and many people with the disease have a life expectancy that's close to the average life expectancy in the general population, according to the Parkinson's Disease Foundation.

"You die with Parkinson's disease, not from it," according to the Michael J. Fox Foundation for Parkinson's Research. Reno's family did not release any further details about her death.

But in some cases, advanced symptoms of Parkinson's disease can lead to complications that result in death, the Michael J. Fox Foundation says. For example, patients can have problems swallowing because they have a loss of control over the muscles in their throat. [3 Myths About Parkinson's Disease]

Swallowing problems can cause patients to inhale small bits of food, which may result in aspiration pneumonia, an infection of the lungs that can be life-threatening. A 1999 study of people with Parkinson's disease that followed patients for 10 years found that pneumonia was the most common cause of death in these patients, causing nearly one-third of all deaths among patients in the study.

Patients also may have impaired balance, which can result in falls that lead to serious or even fatal injuries, the Michael J. Fox Foundation says.

A 2010 study of more than 200 people with Parkinson's disease in Norway found that, on average, patients were diagnosed with the disease at age 65, and lived for 16 years after their diagnosis, to age 81, according to the Parkinson's Disease Foundation. Those who lived with the condition for a shorter time than the average tended to be male, have more severe problems with their movements (in particular, problems with balance and walking) or have symptoms of dementia along with their Parkinson's.

Reno, who was the first female attorney general in the United States, was diagnosed with Parkinson's in 1995 (at age 57), while she was still in office, and she held the position until 2001. She died at her home in Miami-Dade County, Florida, according to The New York Times.

Original article on Live Science.

It was only after actor Robin Williams' death in August 2014 that doctors found the true cause of the symptoms that had plagued him for years, according to Williams' widow, Susan Schneider Williams.

Writing in an editorial published Sept. 27 in the journal Neurology, Schneider Williams detailed the intense difficulty of determining the cause of her husband's symptoms.

After his death, doctors finally determined that Williams had a condition called Lewy body disease, which Schneider Williams described as a "terrorist within his brain." [Top 10 Stigmatized Health Disorders]

Lewy body disease is one of the most common forms of dementia, according to the National Institutes of Health. It occurs when Lewy bodies, or clumps of protein called alpha-synuclein, build up in the brain.

The doctors who examined Williams' brain after his death said that his case was "one of the worst pathologies" they had ever seen, Schneider Williams wrote. "He had about 40 percent loss of dopamine neurons, and almost no neurons were free of Lewy bodies throughout the entire brain and brainstem," she wrote.

But Robin Williams was not diagnosed with Lewy body disease while he was alive. Rather, he received a diagnosis of Parkinson's disease on May 28, 2014, Schneider Williams wrote. Both Lewy body disease and Parkinson's disease involve the presence of Lewy bodies in the brain, according to the editorial.

Robin Williams' clinical symptoms were those of Parkinson's, and his brain pathology showed he had Lewy body dementia, Schneider Williams wrote. Whether a person is diagnosed with Lewy body disease or Parkinson's disease can depend on which symptoms occur first, she wrote.

Indeed, symptoms of Lewy body disease can resemble those of Parkinson's disease, according to the Lewy Body Dementia Association.

Disease progression

Before Williams was diagnosed with Parkinson's disease, he had experienced a wide array of symptoms that seemed unrelated, according to the editorial. [3 Myths About Parkinson's Disease]

By October 2013, Schneider Williams said the actor had been experiencing constipation, urinary difficulty, heartburn, sleeplessness, insomnia, a poor sense of smell and stress. In addition, he had "a slight tremor in his left hand that would come and go," but at the time, that was attributed to a previous shoulder injury, she wrote.

At the end of that October, Williams developed gut pain, and his reaction was "markedly out of character," Schneider Williams wrote. "His fear and anxiety skyrocketed to a point that was alarming," she wrote.

Over the next few months, Williams' symptoms got worse. He had increasing problems with paranoia, delusions, insomnia and memory, as well as high cortisol levels, Schneider Williams wrote. He tried psychotherapy and various medications, she wrote. Later, she learned that a high concentration of Lewy bodies in the part of his brain called the amygdala likely caused the "acute paranoia and out-of-character emotional responses he was having," she wrote.

His neurological symptoms worsened through the spring, and his "loss of memory and inability to control his anxiety was devastating to him," Schneider Williams wrote.

He later developed more physical symptoms typical of Parkinson's disease, including a continuous tremor in his hand and a slow, shuffling gait, according to the editorial. He had terrible insomnia and began having trouble judging distance and depth, Schneider Williams wrote.

In addition, his symptoms could come and go quickly, she wrote. Williams would be "lucid with clear reasoning one minute and then, five minutes later, blank, lost in confusion," she wrote. This fluctuation in symptoms is common in people with Lewy body disease, she added.

Overall, Williams "experienced nearly all of the 40-plus symptoms of [Lewy body disease]," Schneider Williams wrote. Though he never said he had hallucinations, a doctor later told Schneider Williams that he likely did have them but didn't tell anyone.

Originally published on Live Science.

Boxing champion Muhammad Ali lived with Parkinson's disease for three decades before his death on Friday (June 3) at the age of 74, and many have wondered whether Ali's boxing career caused him to develop the neurological disorder.

Although it's likely that frequent head injuries played a role in the boxer's Parkinson's disease, certain genes may have also increased his susceptibility to the disease, experts said.

"[It's] likely his repeated head injuries contributed to his Parkinson's disease," said Dr. Barbara Changizi, a neurologist at The Ohio State University Wexner Medical Center, who was not involved with Ali's treatment. But given how young Ali was when he was diagnosed with the disorder — the boxer was 42 — there's a "strong chance that genetics played a significant role as well," Changizi said. The average age of Parkinson's onset is 60 years old, according to the Michael J. Fox Foundation. [10 Things You Didn't Know About the Brain]

In patients with Parkinson's disease, the brain cells that produce a chemical called dopamine start to die off. Because dopamine is important for the control of muscle movement, Parkinson's patients experience symptoms such as tremors, slowed movements and muscle stiffness.

In most cases, the exact reason that the dopamine-producing cells start to die is not known, Changizi said. But certain genes appear to increase people's risk of developing the disease at a relatively young age. For this reason, "when you have young onset disease, we are more suspicious" of genetics contributing, Changizi said.

Still, head trauma has also been linked with Parkinson's disease. In a 2013 review study, researchers found that people with head trauma that resulted in a concussion were 57 percent more likely to develop Parkinson's disease, than people who never experienced such head trauma.

Head injuries can cause inflammation in the brain, which may lead to changes in cells and brain structures that contribute to Parkinson's, Changizi said.

And injuries that specifically damage the part of the brain that contains dopamine-producing cells, called the substantia nigra, can also lead to Parkinson's, Changizi said.

After Ali's death, some people asked on social media sites whether Ali could have also suffered from chronic traumatic encephalopathy (CTE), a brain disease found in athletes such as football players who have experienced repeated blows to the head.

But Changizi said, "Parkinson's disease would be enough to explain a lot of his symptoms."

The official cause of Ali's death was septic shock, according to news sources. Septic shock is a complication that can happen in people who have an infection. It can involve bodywide inflammation, and a dangerous drop in blood pressure. Ali had been hospitalized a week before he died for a respiratory infection, sources reported.

Original article on Live Science.

Introduction

Botox is typically known as a tool for smoothing out wrinkles, but it actually has many other applications in medicine.

Botox, a trademark that's short for botulinum toxin, is a neuromuscular blocker, which means it paralyzes the muscle into which it is injected, said Dr. Daniel Maman, a board-certified plastic surgeon and an assistant clinical professor of surgery at the Icahn School of Medicine at Mount Sinai in New York. And because muscle issues are involved in many different types of medical conditions, the range of medical applications of Botox has been expanding, he told Live Science. The drug has uses in neurological conditions, such as migraines and drooling from Parkinson's disease.

Here's a look at seven conditions that Botox is used to treat.

Crossed Eyes

The first time Botox was ever used for a medical purpose was in 1981, to treat people with crossed eyes, according to the e-book "Plastic Surgery," by Lana Thompson. In 1989, the U.S. Food and Drug Administration officially approved the use of Botox for this condition.Injecting Botox into muscles that control the movement of the eye reduces the appearance of crossed eyes.

Excessive sweating and body odor

For those who sweat too much or who have trouble reducing their body odor with the use of traditional deodorants, Botox injections may be helpful, research has shown. Normally, sweat is produced when the small muscles around sweat glands squeeze the liquid out, Maman said."And if you can paralyze those small muscles, then the sweat glands are no longer functioning like they normally would," he said.

In a 2007 study published in the journal Dermatologic Surgery, researchers injected Botox into the armpits of 51 people. Both the participants and the independent raters of smell samples from the people's armpits said the people's underarm odor was less unpleasant after they received the injections. Botox was approved by the FDA to treat excessive sweating in 2004.

Chronic pain

Botox may help treat people with myofascial pain syndrome, which is a chronic condition that involves muscle pain.

In a study published in June 2014 in the journal Anesthesia & Analgesia, researchers injected Botox into the painful muscles in the neck and shoulder areas of 114 people with the condition. The researchers found that the people's pain was reduced after they received the injections.

Traditionally, physical therapy and anti-inflammatory drugs like ibuprofen have been used to treat the symptoms of this condition. However, "long-term benefit with traditional therapies is transient and unpredictable," Dr. Andrea L. Nicol, who led the study and is an assistant clinical professor of anesthesiology at UCLA, said in a statement. [5 Surprising Facts About Pain]

Drooling in Parkinson's disease

People with Parkinson's disease, who have problems with their muscle function and may swallow less frequently than normal, sometimes develop excessive drooling. But Botox may help to treat this symptom. In a study published in 2006 in the journal Movement Disorders, researchers administered Botox to the salivary glands of 32 people with Parkinson's disease who had been experiencing excessive drooling. The researchers found that after the treatment, the people drooled less and produced less saliva. The people did not experience any side effects from the Botox, according to the study.

Chronic migraines

Chronic migraine is another condition that Botox may help treat, because certain muscular mechanisms have been implicated in the development of migraines. "Patients with chronic migraine experience a headache more than 14 days of the month," Dr. Russell Katz, director of neurology products at the FDA, said in a statement. "This condition can greatly affect family, work and social life, so it is important to have a variety of effective treatment options available."

The FDA approved the use of Botox for chronic migraine in 2010. To treat the condition, injections of the drug are administered to a person's head and neck area about every 12 weeks. [Ouch: 10 Odd Causes of Headaches]

Overactive bladder

In 2013, the FDA approved Botox to treat adults with overactive bladder who can't use, or who are not helped by, the medications that are normally used in the treatment of this condition.

The bladders of people with this condition squeeze too often, or squeeze without warning, causing them to urinate too frequently or leak urine. Injecting Botox into the bladder causes the bladder to relax, which increases the organ's storage capacity and reduces the frequency of episodes of urinary incontinence, according to the FDA.

Depression

The wide range of applications for Botox use are spreading into psychiatry. In a study published in 2014 in the Journal of Psychiatric Research, researchers administered Botox or a placebo to the muscles in the area between the eyebrows to 74 people with depression.

They found that, among the people injected with Botox, symptoms decreased by 47 percent six weeks after treatment, compared with a 21-percent decrease in the placebo group. Several mechanisms may have been involved in the improvement of mood observed in the study, the researchers noted. For example, greater levels of frowning are believed to contribute to depression symptoms, and the reduction in frowning after the treatment may have put the people in a better mood, according to the study. (Botox is not an FDA-approved treatment for depression.)

Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

A pesticide that was present in milk in the early 1980s may be linked to signs of Parkinson's disease that are showing up in people today, according to a new study.

The researchers looked at Japanese-American men in Hawaii, where the pesticide was frequently used, and found that those who drank more than two cups of milk daily at the start of the study had 40 percent fewer brain cells in an area of the brain called the substantia nigra 30 years later, on average, compared with similar men who drank less than two cups of milk per day.

The loss of brain cells in this area of the brain may be an early sign of Parkinson's disease, and can start decades before any visible symptoms of the disease occur, the researchers said. The study included men whose average age was 54 at the start of the study.

The link between the higher consumption of milk and the loss of cells in this brain area was not found among the men in the study who had ever smoked cigarettes, the researchers noted. Previous research has shown that people who smoke cigarettes may have a lower risk of developing Parkinson's disease, the researchers said. [10 Things You Didn't Know About the Brain]

The researchers also found that residues of the pesticide, called heptachlor epoxide, were present in the brains of 90 percent of the men who drank the most milk, compared with 63 percent of those who did not drink any milk.

High levels of the pesticide were found in the milk supply in the early 1980s in Hawaii, where the chemical was used for insect control in the pineapple industry. The commercial sale of the pesticide in agriculture was banned in the United States by 1988, according to the U.S. Environmental Protection Agency. However, a related compound can still be used today for controlling fire ants in electrical grid machinery, according to the Agency for Toxic Substances & Disease Registry.

The researchers noted that they do not have direct evidence that the milk the men drank contained the pesticide. However, they "just have no other explanation for how heptachlor epoxide found its way into the brains of men who consumed milk," said study author Robert D. Abbott, of the Shiga University of Medical Science in Otsu, Japan.

In the study, researchers followed about 450 Japanese-American men for more than 30 years until they died, and then performed autopsies on them. They looked at the cells in the substantia nigra, and also measured the amount of the pesticide residue in 116 of the men's brains, according to the study, published today (Dec. 9) in the journal Neurology.

The findings suggest that diet may play a role in the development of Parkinson's disease, the researchers said. However, the new results do not show a cause-and-effect relationship between the pesticide or milk and Parkinson's disease. Rather, they show there is an association between these factors, they said.

"The vast majority of milk consumers do not get Parkinson's disease," Abbott told Live Science.

But Abbott recommended that people should generally be vigilant about eating food that may contain pesticides. 

Dr. Honglei Chen, of the National Institute of Environmental Health Sciences, who was not involved in the study, said that the association found in the study could potentially be explained by mechanisms other than this pesticide actually causing the brain changes.

Chen, who wrote an editorial on the findings that is also published today in the journal, noted that the men's milk consumption was measured only once at the start of the study. The study assumes that "this measurement represented participants’ dietary habits over time," but this may not have been the case, he said in a statement.

Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Although actor Robin Williams died by suicide, the underlying cause of his death was a rare brain disease called Lewy body dementia, according to his widow.

The disease caused Williams to experience hallucinations and other debilitating neurological symptoms, including depression, Susan Schneider Williams, widow of the late actor, told People magazine in a recent interview. An autopsy released in 2014 confirmed that the actor had the disease, but this is the first time that his condition has been discussed in detail.

"It was not depression that killed Robin," Schneider Williams said in the interview. "Depression was one of, let's call it 50 symptoms, and it was a small one."

But whereas other neurological disorders are well known, few people have heard of Lewy body dementia. Though the disease can cause symptoms similar to those seen with Alzheimer's disease, Lewy body dementia is caused by the abnormal buildup of a different protein from the one that is linked with Alzheimer's. [10 Ways to Keep Your Mind Sharp]

Lewy body dementia

Lewy body dementia was discovered in the early 1900s, when researcher Frederic Lewy, who worked in the laboratory of neurologist Alois Alzheimer, found the abnormal buildup in the brain tissue of dementia patients.

Today, the disease affects 1.4 million Americans, according to the Lewy Body Dementia Association. A 2013 study in the journal Archives of Neurology (now JAMA Neurology) found that men are about twice as likely as women to develop the disease.

The condition occurs when Lewy bodies, or clumps of a protein called alpha synuclein, build up in the brain. No one knows why Lewy bodies accumulate, but they are also found in the brains of people with Parkinson's disease, and in the brains of those with Alzheimer's.

Myriad symptoms

Lewy body dementia can cause visual hallucinations; rigid movements and motor problems similar to those found in people with Parkinson's disease; sleep disorders; anxiety; interruptions in the ability to pay attention; and loss of memory, according to the National Institute on Neurological Disorders and Stroke. As in Williams' case, the disease can also fuel depression.

Lewy body dementia can mimic other diseases, such as Parkinson's disease and Alzheimer's disease. Researchers are still trying to figure out how Parkinson's disease and Lewy body dementia may be related. Although abnormal processing of alpha-synuclein plays a role in both diseases, Parkinson's disease seems to preferentially occur in a brain area called the substantia nigra, an almond-shaped region in the mid-brain responsible for reward, addiction and movement, whereas Lewy body dementia tends to occur more diffusely, throughout the brain, according to the Alzheimer's Association.

Still, up to 80 percent of Parkinson's patients go on to develop some type of dementia, according to the Alzheimer's Association.

Currently, if people develop the movement disorder known as Parkinsonism and then do not develop dementia within a year, they are diagnosed with Parkinson's disease. If they do develop dementia within the year, their condition is classified as Lewy body dementia, according to the Alzheimer's Association.

There is no cure for Lewy body dementia, and the disease is progressive, meaning it gets worse over time. Most treatments focus on controlling symptoms, such as hallucinations or sleep disturbances. However, a 2010 study published in the journal The Lancet Neurology found that a drug called memantine, which is used to slow the loss of cognitive abilities in people with Alzheimer's, can also improve symptoms in people with Lewy body dementia and Parkinson's disease.

People with Lewy body dementia typically live about eight years after their diagnosis, according to the National Institute on Neurological Disorders and Stroke.

Follow Tia Ghose on Twitterand Google+. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

In a case that has mystified doctors, a professional artist who developed Parkinson's disease and then suffered a debilitating arm injury managed to continue to paint with his other arm ­— just as well as he had painted with his good arm, according to a new report.

Doctors diagnosed Juan Mallol Pibernat, a Spanish artist, with Parkinson's disease when he was in his early 70s. The illness causes the loss of brain cells in an area that controls muscle movement, and symptoms can include tremors, impaired balance and coordination, and limb stiffness, according to the National Institutes of Health.

One day, Mallol Pibernat lost his balance while carrying one of his works. In trying to avoid falling on his painting, he landed on his right arm instead, fracturing it, according to the report of his case, published online June 8 in the journal Neurocase: The Neural Basis of Cognition.

Doctors put the artist in a cast for 40 days, but that didn't stop Mallol Pibernat. He had agreements in place for commissioned paintings, and didn't want to disappoint his clients, so he painted with his unpracticed left hand, said co-author of the case report Dr. Kuan Kho, a neurosurgeon at Medisch Spectrum Twente hospital in the Netherlands.

Painting with a nondominant hand requires a brain structure that is impaired in people with Parkinson's, Kho said. But, curiously, Mallol Pibernat painted with his left hand for the next five weeks, and the quality of his paintings was "comparable to the works he made with his right hand," the doctors wrote in the report. [3 Myths About Parkinson's Disease]

The artist has since recovered from the fracture, and now paints with his right hand again, the doctors added.

Sleight of hand

Kho said he was impressed that Mallol Pibernat could paint well with his nondominant hand, a task that would be difficult even without Parkinson's disease. "Have you ever tried painting or drawing with your nondominant hand?" Kho said. "It's hard."

Doctors call such a switch, in which a person learns a motor skill with one hand and is able to transfer it to the other, "intermanual transfer." Studies show that intermanual transfer means that people don't have to learn a new skill from scratch when they switch hands; for instance, people might master a motor skill more quickly in one hand if the other hand learned it first, Kho said.

However, Parkinson's disease disrupts a part of the brain involved in intermanual transfer, Kho said. This area, called the supplementary motor area, helps people initiate movement and learn new motor skills.

Mallol Pibernat's case is intriguing because "it shows that even with Parkinson's disease, you can move some skills from one hemisphere [of the brain] to another hemisphere," Kho said. "Why that is, I have no clue at this moment."

It's possible that intermanual transfer of motor skills uses other brain structures in addition to the supplementary motor area, Kho said. If Parkinson's disease does not affect these other structures, that could explain Mallol Pibernat's mystifying accomplishment.

Another possibility is that the artist's Parkinson's medication had restored the neural activity in the supplementary motor area to typical levels, allowing for the skill transfer, Kho said.

Both of these ideas are compelling, but Mallol Pibernat may just be a man of extraordinary talent, said Dr. Paul Wright, the chairman of neurology at North Shore University Hospital and Long Island Jewish Medical Center in New York, who was not involved with the case report.

The case study highlights the need for researchers to learn more about how Parkinson's disease and motor learning interact, both Kho and Wright said. It also demonstrates how harmful falls are, and how "we have to always do everything possible to avoid falls," Wright said.

Moreover, it would be interesting to see whether other people with Parkinson's also experience intermanual transfer, Kho said. Usually, the tremors associated with Parkinson's affect one side of the body more than the other, he said.

"If you could treat patients to use their better side do some things they used to do with their worse side, it might be of practical help," he said.

Follow Laura Geggel on Twitter @LauraGeggel. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

People who have problems with their sense of smell may be at increased risk for dying sooner than those who don't have trouble smelling, a new study suggests.

Researchers analyzed information from more than 1,100 adults in New York City whose average age was 80. The participants took a "scratch and sniff" test in which they attempted to identify 40 common odors. People who scored less than 18 points out of 40 were said to have anosmia, or an inability to smell.

The study found that the people with scores in the low range (zero to 20 points) were nearly four times more likely to die over a four-year period than those with scores in the high range (31 to 40 points). About 45 percent of participants with scores in the low range died during the study period, compared with 18 percent of those with scores in the high range. [7 Ways the Mind and Body Change with Age]

The results held even after the researchers took into account factors that could affect people's risk of death, such as age, alcohol use, head injury, smoking or having dementia.

Therisk of death "increased progressively with worse performance in the smell identification test and was highest in those with the worst smelling ability," study co-author Dr. Davangere Devanand, a professor of psychiatry and neurology at Columbia University, said in a statement.

The results agree with those of a study published last year, which also found a link between smell loss and an increased risk of dying in older adults.

People tend to perform worse on smell tests as they age, and impairments in sense of smell have been linked with Alzheimer's and Parkinson's disease. But the new study suggests that dementia and other medical conditions, by themselves, are not enough to explain the link between problems with smell and increased risk of death.

The researchers noted that a loss of sense of smell could put people at risk for certain hazards, such as ingestion of spoiled food or an inability to smell a natural gas leak or a fire.

A loss of a person's sense of smell may also mean that the cells in the individual's body are not able to regenerate as well as they used to (since the cells responsible for smell detection regenerate throughout life). This could put a person at higher risk of death from other causes.

There remains a need for larger studies looking at whether other factors may explain the link, the researchers said. More work is also needed to determine if the same link can be found in younger populations, the researcher said.

The study is published today (June 3) in the journal Annals of Neurology.

Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

People who have been diagnosed with depression may have an increased risk of developing Parkinson's disease later on, a new study suggests.

In the study, researchers looked at about 140,000 people who had been diagnosed with depression between 1987 and 2012. They matched each of them with three people of the same age and gender who had not been diagnosed with depression. The people in the study were all at least 50 years old by 2005.

The investigators followed the participants for 26 years, and found that 1 percent of the people with depression developed Parkinson's disease, whereas 0.4 percent of the people without depression developed the disease.

The researchers noted that Parkinson's disease is not common, even among people with depression. "Only a very little proportion of those with depression develop Parkinson's disease," said study author Peter Nordström, of Umeå University in Umeå, Sweden. [3 Myths About Parkinson's Disease]

Still, the link should be studied further because the new study adds to the growing body of research connecting Parkinson's disease with certain other health conditions and personality traits. For example, a 2012 study presented at the American Academy of Neurology meeting that year showed that people who are cautious and avoid taking risks are more likely to develop the disease.

Parkinson's disease results from a loss of the brain cells that produce the chemical dopamine. The condition affects body movements — it causes tremors, rigid muscles and impaired balance. About 1 million people in the U.S. have Parkinson's, according to the Parkinson's Disease Foundation.

The new study also suggested that people who have depression and develop Parkinson's do so earlier than people who have not been diagnosed with depression. The people who had depression were 3.2 times more likely to develop Parkinson's disease within a year after the study started, compared with people who did not have depression.

Moreover, the more severe a person's depression, the greater their likelihood of developing Parkinson's disease. For example, people who had been hospitalized for depression were more than three times more likely to be diagnosed with Parkinson's disease than those who had depression but had not been hospitalized because of it. People who had been hospitalized for depression five times or more were 40 percent more likely to be diagnosed with Parkinson's disease than those who had been hospitalized for depression once.

It is not clear whether depression might cause Parkinson's disease, the researchers said. It is possible that depression affects the brain in some way that contributes to the likelihood of developing Parkinson's disease, Nordström told Live Science.

It could also be that the drugs used to treat people with depression, such as antidepressants or antipsychotics, raise a person's risk of developing the disease. Alternatively, depression may be a symptom that precedes the manifestation of Parkinson's disease, the researchers said.

The study was published today (May 20) in the journal Neurology.

Follow Agata Blaszczak-Boxe on Twitter. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

A rare sleep disorder that makes people act out their dreams may be an early warning of a deadly neurological illness, a new review of previous research suggests.

About half of people who have a condition known as rapid eye movement sleep behavior disorder will develop Parkinson's disease or a related disorder within a decade of being diagnosed with RBD.

Eventually, nearly everyone with RBD will ultimately develop a neurological disorder, the study found. [Top 10 Spooky Sleep Disorders]

"If you get this disorder and live long enough, you will almost certainly get Parkinson's disease or a condition similar to it — it's an early warning sign," said Dr. Michael Howell, a professor of neurology at the University of Minnesota in Minneapolis and co-author of the study, published today (April 13) in the journal JAMA Neurology.

The main symptom of RBD is moving around during the rapid eye movement (REM) period of sleep, when most dreaming occurs and the muscles are usually paralyzed by the brain stem. People with RBD are thought to have a brain-stem malfunction that allows them to move during REM sleep, and thus act out their dreams, according to the study.

People with RBD describe having vivid dreams, and their enactments range from small hand movements to violent actions such as punching, kicking or leaping out of bed. The disorder poses a risk of injury to the patient or their bed partner, Howell said. Scientists first described the disorder in the 1980s. It is distinct from sleepwalking, and affects about 0.5 percent of the population, or 35 million people worldwide, he said.

To find out whether RBD was, in fact, an early sign of Parkinson's disease and similar brain disorders, Howell and his colleagues sifted through more than 500 studies on the subject published between 1986 and 2014.

Strikingly, they found that between 81 and 90 percent of patients with RBD developed a degenerative brain disorder during their lifetimes, the studies showed.

Parkinson's disease is caused by the breakdown of certain proteins, called alpha-synuclein proteins, in neurons in the brain that produce dopamine, a chemical that produces pleasurable feelings in response to rewarding activities. It could be that RBD results from the early stages of alpha-synuclein breakdown in the brain, so it could be a useful warning sign of Parkinson's, Howell said. Not everyone who develops Parkinson's disease will have RBD first, however.

The findings could help doctors find a way to treat Parkinson's while it's still in its early stages, Howell said.

RBD is not curable, but it can be treated with high doses of the sleep aid melatonin or low doses of the anti-anxiety drug clonazepam. Patients with RBD should also take steps to prevent possible sources of injury.

"It's very important to make the bedroom environment [as] safe as possible" by removing objects that can be picked up or used as a weapon, such as guns, Howell said.

Parkinson's disease is not curable, either, but it can be managed with drugs. In addition, an experimental therapy known as deep-brain stimulation has shown promise in some patients.

Follow Tanya Lewis on Twitter. Follow us @livescience, Facebook & Google+. Original article on Live Science.

WASHINGTON — Sound body, sound mind, the saying goes. Now, scientists have found support for this adage in researching showing that poor diets may adversely affect mental health in all stages of life, from fetal development through old age.

Studies presented here today at the Society for Neuroscience annual meeting find that the typical, modern Western diet, when consumed by the mother, may hinder the development of a baby's brain while still in the womb. That same diet can lead to depression among adolescents, and contribute to dementia and Parkinson's disease in older adults.

One study examined a high-fat diet in pregnant monkeys. Researchers at the Oregon National Primate Research Center in Beaverton, Oregon, found that baby monkeys exposed to a high-fat diet in the womb were born with fewer dopamine fibers and receptors in a brain region called the prefrontal cortex.

Because dopamine helps regulate the brain's food-reward pathway, these monkeys grew up craving more flavorful, high-fat, high-calorie foods to satiate their appetites, said lead author Dr. Heidi Rivera, a researcher at the center. As a result of this behavior change, the monkeys built up excess fat tissue early on, and such fat is hard to shed. [3D Images: Exploring the Human Brain]

In a similar study on mice, presented here on Monday, Duke University researchers found that a mother's high-fat diet triggers brain inflammation in the developing fetus, leading to anxiety and hyperactivity in the offspring. This supports observations in humans that obesity in pregnancy is associated with childhood attention deficit hyperactivity disorder (ADHD), said Dr. Staci Bilbo of Duke, who led the study.

Diet and the teenage brain

Turning from in-utero development to the teenage years, researchers at Emory University School of Medicine in Atlanta found that a high-fructose diet may exacerbate depressive-like symptomsin adolescents.

Fructose, or fruit sugar, is found naturally in fruits and vegetables but is added in unnatural amounts to beverages and processed foods, often the staples of the teenage diet. A team led by graduate student Constance Harrell found that rats fed a high-fructose diet for 10 weeks showed an altered hormonal response to stress at a genetic level. The response was consistent with what is seen in people with depression.

Harrell said that such a profound dietary effect is of particular concern during the human teen years, a critical time for the development of the brain's stress response.

Obesity and dementia

Researchers from the Australian National University found that the obesity epidemic may be contributing to the dementia epidemic. A study led by Dr. Nicolas Cherbuin followed 420 cognitively healthy adults who were in their early 60s at the study's start. Over an eight-year period, the team tracked changes in the participants' body weight as well as the size of each person's hippocampus, a region in the brain critical for long-term memory.

As estimated from brain scans, the hippocampus shrunk with each pound packed on at a rate of 7.2-percent shrinkage for every 2-point increment in BMI (body-mass index, a measure of obesity). Normal shrinkage at this age is only about 0.5 to 1 percent, Cherbuin said.

The study adds to other observational evidence that "being overweight or obese is associated with poorer brain health in older adults," Cherbuin said. "Obesity is associated with a two-fold increased risk of dementia and 60-percent increased risk of Alzheimer's disease," he added. Those results are based on his earlier research findings.

Calorie restriction has been shown to slow the aging process in mice and monkeys. Now, researchers at Monash University in Melbourne, Australia, have identified a hormone that may provide the same benefits, only without the need to so drastically reduce what people eat.

The hormone is ghrelin, the so-called "hunger hormone" that helps regulate appetite. The Monash team worked with mice that were placed on a calorie-restricted diet and were genetically engineered so that they would not produce ghrelin. These mice did not live longer than mice that were not on a diet, demonstrating that ghrelin may be a key element in providing longevity benefits in such a diet.

The researchers then injected ghrelin in mice with Parkinson's disease and found changes in the animals' brains associated with a decrease in cell loss from Parkinson's.

Jacqueline Bayliss, a graduate student who presented the study, stressed that this is an early phase of research, however promising for the treatment of Parkinson's.

Together, these independent studies "demonstrate the complex effects that diet and obesity have on brain health, mental function and behavior," said Dr. Ralph DiLeone of Yale University, an expert in neurobiology who was not associated with any of the presented research. "[D]eepening our understanding of those relationships … may eventually lead to better treatments for many neurological disorders."

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.

Pathological gambling, hypersexuality and compulsive shopping are some of the abnormal behaviors that are linked to the use of certain drugs commonly used to treat Parkinson's disease, according to a new study.

The findings are important because they mean that doctors and patients should be wary of the drugs' side effects, according to the study authors. But they also give researchers a better understanding of how abnormal behaviors develop in general, and how such behaviors may be related to the brain receptor that is targeted by the drug, the authors said.

"In our view, these medications should be used less frequently and with great caution, paying close attention to possible untoward effects on behavior and impulse control," said Dr. Howard D. Weiss of Sinai Hospital of Baltimore and Dr. Gregory M. Pontone of Johns Hopkins University School of Medicine in Baltimore, Maryland, writing in an editorial about the new study.

In the study, the researchers examined 1,580 reports of people in the United States and 21 other countries experiencing pathological gambling, hypersexuality, compulsive shopping or other abnormal behaviors after taking medication between 2003 and 2012. They found that 710 of the cases occurred in people taking drugs called dopamine receptor agonists, which are used to treat Parkinson's disease, whereas the other 870 cases occurred in people taking all of the other types of drugs combined.  

The researchers determined that the proportion of such reports was 277.6 times higher for people taking dopamine agonist receptor drugs than those taking other drugs. [7 Bizarre Drug Side Effects]

Dopamine is a neurotransmitter in the brain that normally helps regulate movement, emotions and the feelings of pleasure. In people with Parkinson's disease, the brain cells that make dopamine die over time. Dopamine receptor agonists are used to mimic the function of the neurotransmitter.

The important step to take after the new findings is to introduce warnings about the potential side effects of those drugs so that doctors who prescribe them are aware of them, said study author Thomas J. Moore, a senior scientist at the Institute for Safe Medication Practices in Alexandria, Virginia.

"They [doctors and caregivers of Parkinson's patients] need to be on the lookout for this kind of behavior" and understand it may be linked to the use of medication, Moore told Live Science.

Of all the cases of abnormal behavior that were observed in the people taking the drugs for Parkinson's disease, the majority (410 cases) occurred in those who had been taking a dopamine receptor agonist drug called pramipexole, which affects a receptor called dopamine D3 receptor. And the drug that was second-most commonly linked to such behaviors was ropinirole, which also has a significant effect on the D3 receptor, according to the study, published today (Oct. 20) in the journal JAMA Internal Medicine

The researchers noted that in some cases, the people taking these drugs had restless leg syndrome (not Parkinson's disease).

The new research may allow researchers to better understand how abnormal behaviors develop, and how they may be related to the D3 receptor, Moore said. The D3 receptor has also been investigated as a possible target for treatments for people with addictions, the researchers wrote in the study.

In another study, published in July 2011 in the journal Physiology & Behavior, other researchers also found a link between behaviors such as hypersexuality or excessive gambling and the use of the two drugs that Moore found to be the most closely related to abnormal behaviors in the new study.

Drugs for Parkinson's have been down this road before. In the 1960s, the introduction of the Parkinson's drug levodopa enabled Parkinson's patients to “regain function and return to the mainstream of life," Weiss and Pontone wrote.

Levodopa gets converted into dopamine in the brain, said Weiss and Pontone, who were not involved with the new research.

However, enthusiasm for that treatment was tempered when patients taking it developed involuntary muscle movements, similar to tics, and in rare cases also developing abnormal behaviors such as hypersexuality, they wrote.

The newer class of Parkinson's drugs — the dopamine receptor agonist drugs — act differently in the brain, Weiss and Pontone wrote. Levodopa gets converted into dopamine in the brain, the dopamine receptor agonist drugs just mimic the neurotransmitter's effects.

It was known that the dopamine receptor agonist drugs caused side effects such as hallucinations, psychosis and excessive daytime sleepiness. But despite these effects, the drugs remain widely used, and it is only recently that doctors started recognizing a link between the use of those drugs and the occurrence of impulse control disorders with symptoms such as pathological gambling, hypersexuality and uncontrollable spending, Weiss and Pontone wrote.

It is not surprising that it took a while for doctors to start recognizing the link between the two, they wrote, as they did not routinely inquire about the potentially behavior-altering effects of the drugs.

"During an office visit, a patient is unlikely to spontaneously mention, 'By the way, doctor, I lost $250,000 in casinos last year, and I purchase $500 of lottery tickets every week' or 'I spend all night on Internet pornography sites and am soliciting prostitutes,'" Weiss and Pontone noted.

"In summary, physicians have overestimated the benefit and underestimated the risks associated with the use of dopamine receptor agonist drugs in patients with Parkinson disease," they wrote.

Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science.

Actor Robin Williams was experiencing the early symptoms of Parkinson's disease before he committed suicide on Monday, according to news reports.

In a statement, Williams' widow, Susan Schneider, said that her late husband had been struggling with the early stages of Parkinson's disease, but was not ready to share his diagnosis with the public, according to USA Today.

"Robin's sobriety was intact, and he was brave as he struggled with his own battles of depression, anxiety as well as early stages of Parkinson's disease, which he was not yet ready to share publicly," Schneider's statement said.

"It is our hope, in the wake of Robin's tragic passing, that others will find the strength to seek the care and support they need to treat whatever battles they are facing so they may feel less afraid," the statement said.

Parkinson's disease causes the loss of brain cells in a part of the brain that controls muscle movement. Symptoms can include tremors, stiffness in the arms and legs, and impaired balance and coordination, according to the National Institutes of Health. [3 Myths About Parkinson's Disease]

Symptoms usually appear gradually, and as the diseases progresses, it can interfere with daily activities, the NIH says. There is no cure for Parkinson's disease, but medications can provide relief from symptoms, the NIH says.

Most people with the condition are diagnosed after age 60, but about 10 percent receive a diagnosis before age 40, according to the National Parkinson's Foundation. Williams was 63.

Some studies have looked at whether there is a link between Parkinson's disease and an increased risk of suicide, but have not found one. A 2007 study conducted in Denmark found that the rate of suicide among people with Parkinson's disease was about the same as that of the general population.

A 2001 study in the United States that included more than 144,000 people with Parkinson's disease found that the rate of suicide in the general population was about 10 times higher than the rate of suicide among people with Parkinson's disease.

However, a 2008 study found a higher-than-expected rate of suicide among people with Parkinson's disease who had undergone a treatment called deep brain stimulation for their condition. Deep brain stimulation involves surgery to implant a device that sends electrical impulses into the brain. In this study, suicide was more likely in participants who had depression, or who were single. (There are no reports that Williams underwent deep brain stimulation.)

Typically, the treatment is used for people with advanced Parkinson's disease, and is only recommended if patients do not respond to medication.

Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

A woman with Parkinson's disease took a drug commonly used for people with the condition and began experiencing unwanted, spontaneous orgasms, according to a new report of her case.

The 42-year-old woman with early-onset Parkinson's disease was admitted to the hospital complaining about the orgasms. She said she had been taking the drug rasagiline for 10 days, and on the seventh day, she started experiencing hyperarousal and increased libido, according to the case report.

She then experienced three to five orgasms daily, each of which lasted from five to 20 seconds.

"Here we report a patient with early-onset PD [Parkinson's disease] who experienced spontaneous orgasms when taking rasagiline; these were unwelcome and occurred in the absence of hypersexual behavior," the researchers from the department of neurology at Necmettin Erbakan University in Konya, Turkey, who treated the woman, wrote in the study.

"To the best of our knowledge, this is the first report of this adverse effect of rasagiline," they wrote.

How a drug can cause orgasms

The woman had not been taking any other medication, and she did not experience any other unusual symptoms related to the use of the drug, according to the report. She then stopped taking the medication because of the orgasms, but when she started taking it again 15 days later, the spontaneous orgasms occurred again, so she stopped for good. [10 Surprising Sex Statistics]

Typical side effects of rasagiline include flulike symptoms, joint pain, depression and gastric problems, the researchers wrote in the study.

It is not clear why exactly the drug seemed to trigger this unusual reaction, the researchers wrote. However, they suspected that it had something to do with an increase in dopamine, which is a neurotransmitter in the brain that helps regulate the feelings of pleasure, and is triggered by taking rasagiline. (In people with Parkinson's disease, the cells that normally make dopamine die over time.)

There have also been reports of orgasms induced by other drugs, such as certain antidepressants, which act on the central nervous system, the researchers wrote in their report.

And one previous report described a case of a spontaneous ejaculation in a man who had also been taking rasagiline, they wrote.

"There are indeed other drugs that can stimulate sexual response," said Barry Komisaruk, a distinguished professor at Rutgers University in New Jersey, who researches orgasms.

Just like rasagiline, many of these drugs activate dopamine, which is also released during orgasm, Komisaruk said.

The dopamine link

The importance of dopamine in human orgasms was initially recognized when researchers noticed signs of increased sexual arousal in male nursing home patients who had been taking L-DOPA, another dopamine-inducing drug used in the treatment of Parkinson's disease, Komisaruk told Live Science.

"It is also fairly well known that cocaine can mimic the effect of orgasm," through its effect on the levels of dopamine, he said.

The case report will be published in an upcoming issue of the journal Parkinsonism and Related Disorders.

Follow Agata Blaszczak-Boxe on Twitter. Follow LiveScience @livescience, Facebook & Google+. Originally published on Live Science.

People with Parkinson's disease may have higher levels of creativity than their healthy peers, a new study finds.

Researchers compared the creativity levels of 27 Parkinson's patients with 27 healthy people of the same education level and age. Participants were asked to interpret abstract pictures, answer questions aimed at provoking imagination (such as, "What can you do with sandals?") and explain imaginative metaphors such as a "scarf of fog."

The researchers found Parkinson's patients understood more of the pictures, brainstormed more metaphors with symbolic meaning rather than literal meaning and drew a larger number of interpretations from abstract images, compared with the people without Parkinson's.

Study researcher Rivka Inzelberg, a neurologist at Tel Aviv University's Neuroscience Center, said that Parkinson's patients often feel liberated from the illness when they are allowed to engage in creative activities, which can be good for their well-being. Although Parkinson's patients have difficulty moving, they can feel differently when they paint; some describe their motions as feeling big, as if they didn't have the illness, Inzelberg said.

From the artist Vincent Van Gogh's supposed episodes of manic, passionate painting, to the hallucinations and anxiety that may have plagued Edvard Munch, who painted the famous work of art "The Scream," researchers have long observed a connection between neurodegenerative or mental disorders and surges in creativity. [In Photos: Van Gogh Masterpiece Reveals True Colors]

Inzelberg said her research began after she noticed a large number of case studies of people with Parkinson's disease who developed a passion for the visual arts or writing.

The researchers also found that the Parkinson's patients who took higher doses of their medication gave even more creative answers than their less-medicated peers. That finding suggests that the medication, which boosts dopamine in the brain, may cause creativity to spike as well.

The reason for the link isn't clear, but one idea is that people with Parkinson's have low levels of the dopamine hormone, and their medication provokes a surge in both the hormone and creativity, Inzelberg said. She noted this would only be true of people who had Parkinson's disease to begin with.

A second theory posits that "when some parts of the brain are degenerating, other parts are becoming more active, and talents can emerge," Inzelberg told Live Science.

The creativity of Parkinson's patients may resemble what scientists have observed in patients with another neurodegenerative disorder called Frontotemporal Dementia (FTD), a disease similar to Alzheimer's. Many case studies show that patients with FTD develop a sudden desire to produce art, said Dr. Anjan Chatterjee, a neurology professor at the University of Pennsylvania.

In 2005, researchers at University College London observed a person who, after a brain hemorrhage, began to obsessively sketch hundreds of faces and drawings as large as rooms, said Chatterjee, who was not involved in the study.

"We have the tendency to think of neurological disorders in the context of people's deficit, but it is also helpful to think of ways in which they have preserved or, in some instances, enhanced abilities," Chatterjee told Live Science. "Art-making is one of the fewest if not the only behavior that in some cases does improve [in] the instances of neurological disease."

Follow Jillian Rose Lim @jillroselim & Google+. Follow Live Science @livescience, Facebook& Google+. Original article on Live Science.

Several studies have linked pesticides with the development of Parkinson's disease, and now a new study has found a specific gene that may explain why some people are particularly susceptible to developing Parkinson's after exposure to certain pesticides.

Parkinson's disease results from the loss of neurons involved in processing the neurotransmitter dopamine. Researchers had previously found a gene that was involved in dopamine processing, and in animal experiments, they determined which pesticides inhibited this gene's pathway.

In the new study, they found that one variant of the gene, called ALDH2, may be even more susceptible to inhibition from pesticides. They then tested for this gene variant in Californians with Parkinson's disease whose exposure to various pesticides could be measured by comparing where they had lived with charts of pesticide use in the state.

The findings show that for people with certain genes, exposure to pesticides may increase the risk of developing Parkinson's disease two to six times, the researchers said.

"We should be much more careful in our industrial agriculture with the agents we're putting out in the environment," said study author Dr. Beate Ritz, a professor of epidemiology at University of California, Los Angeles and co-director of the school's Center for Gene-Environment Studies in Parkinson's Disease. "All of this is environmental exposure, not occupational exposure. It can be quite harmful."

Ritz told Live Science that the study had two goals: to find out which genes might be involved in the nerve death that results in Parkinson's, and to see if there was a variant of that gene that could be found in people exposed to pesticides who developed Parkinson's. [10 Things You Didn't Know About the Brain]

There were four pesticides the researchers found that appear to trigger an effect on enzymes called neuronal aldehyde dehydrogenases (ALDHs), which are involved in processing the brain chemical dopamine.

The researchers then looked at exposure to those four pesticides in a group of 360 people with Parkinson's who lived in central California, and a control group of 953 people who lived in the same area and had similar pesticide exposures but had not developed Parkinson’s. They found that pesticide exposure increased the risk of Parkinson’s, and the risk was further increased among people with a variant of the ALDH2 gene.

Though researchers were able to identify four pesticides that might be responsible for this effect, they were not able to identify a specific pesticide as the culprit.

One important part of the study, Ritz said, was that the researchers had maps of pesticide use from the past 40 years available because of California laws requiring that pesticide use be reported. It would be difficult or impossible to repeat the study in another state, she said.

Going forward, there are two approaches to take, Ritz said. One is that certain pesticides may need to be further scrutinized or banned because of their potential harm, she said.

Another step that should be taken is to see whether a treatment can be created to reduce the susceptibility of certain people to Parkinson's if they have the gene variant.

"Can we predict who might develop Parkinson's? Would they want to take meds? These are questions we need to answer," Ritz said.

The study is published online today (Feb. 3) in the journal Neurology.

Follow Joe Brownstein @joebrownstein. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.

This Behind the Scenes article was provided to LiveScience in partnership with the National Science Foundation.

The poster child for basic research might well be a one-celled green algae found in ordinary lakes and ponds. Amazingly, this unassuming creature — called Chlamydomonas —is helping scientists solve one of the most complex and important mysteries of science: How billions of neurons in the brain interact with one another through electrochemical signals to produce thoughts, memories and behaviors and how malfunctioning neurons may contribute to brain diseases such as Parkinson's disease and schizophrenia.

It may seem counterintuitive that a tiny, relatively simple organism that doesn't even have a brain could help scientists understand how the brain works. But this algae's value to brain scientists is not based on its intellect. Rather, it is based on its light-sensitivity, i.e., the fact that this organism's movements are controlled by light.

Following the Light

Chlamydomonasis light sensitive because it must detect and move towards light to feed itself through photosynthesis. You've seen this type of light sensitivity in action if you've ever noticed algae accumulate in a lake or pond on a sunny day.

The secret to the Chlamydomonas's light-chasing success is a light-sensitive protein, known as a channelrhodopsin, which is located on the boundary of the algae's eye-like structure, called an eyespot.

When hit by light, this light-sensitive protein — acting much like a solar panel — converts light into an electric current. It does so by changing its shape to form a channel through the boundary of the eyespot. This channel allows positively charged particles to cross the boundary and enter the eyespot region. The resulting flow of charged particles generates an electric current that, through a cascade of events, forces the algae's two flagella — whip-like swimming structures — to steer the organism towards the light.

The light-sensing proteins of Chlamydomonasand their ability to generate electric currents for light chasing were discovered in 2002 by a research team at the University of Texas Health Science Center at Houston that was led by John Spudich and included Oleg SIneshchekov and Kwang-Hwan Jung; the team was funded by the National Science Foundation. This team's discoveries about the algal proteins followed decades of research by Spudich, a biophysical chemist, and his collaborators on how light-sensing receptors control swimmingbehavior in many types of microorganisms.

"My interest in Chlamydomonas was derived from my interest in the basic principles of vision. That is, the molecular mechanisms by which organisms use light to obtain information about their environment," says Spudich. "I have long been fascinated with how microorganisms 'see' the world and started with the simplest--bacteria with light-sensitive movements (phototaxis), followed by phototaxis in more complex algae. Our focus throughout has been on understanding the basic biology of these phenomena."

When Spudich's research on light sensing by Chlamydomonas was published, it significantly advanced the basic science of light sensing and signaling in microorganisms. But at the time, no one knew that it would eventually serendipitously catapult forward the seemingly far-flung field of brain research.

Identifying the Functions of Neurons

Nevertheless, Spudich's discovery of the light-sensitive algal proteins was a game-changer for an NSF-funded team of brain researchers at Stanford University that was comprised of Karl Deisseroth, Edward Boyden and Feng Zhang. Working together in a uniquely interdisciplinary team during the early 2000s, these researchers collectively offered expertise in neuroscience, electrical engineering, physiology, chemistry, genetics, synthetic biology and psychiatry. (Boyden and Zhang are now at MIT.)

A primary goal of this team was to develop a new technology for selectively turning on and off target neurons and circuits of neurons in the brains of laboratory animals, so that resulting behavioral changes could be observed in real time; this information could be used to help identify the functions of targeted neurons and circuits of neurons.

The strategy behind this technology — eventually dubbed optogenetics — is analogous to that used by someone who, one by one, systemically turns on and off the fuses (or circuit breakers) in a house to identify the contribution of each fuse (or circuit breaker) to the house's power output.

An On/Off Switch for Neurons

But unlike household fuses and circuit breakers, neurons don't have a user-friendly on/off switch. To develop a way to control neurons, the Stanford team had to create a new type of neuronal switch. With funding from NSF, the team developed a light-based switch that could be used to selectively turn on target neruons merely by exposing them to light.

Why did the team opt for a light-based strategy? Because light — an almost omnipresent force in nature — has the power to turn on and off many types of important electrical and chemical reactions that occur in nature including, for example, photosynthesis. The team therefore reasoned that light might, under certain conditions, also have the power to turn on and off electrochemical signaling from brain neurons.

But to create a light-based neuronal on/off switch, the team had to solve a big problem: Neurons are not naturally light sensitive. So the team had to find a way to impart a subset of neurons with light sensitivity (without altering non-target neurons), so that treated neurons would selectively respond to a light-based switch. One potential strategy: to install in target neurons some kind of light sensitive molecule that is not present elsewhere in the brain.

The team lacked the right type of light-sensitive molecule for the job until several important studies were announced. These studies included Spudich's discovery of the light-sensitive algal proteins, as well as research led by microbial biophysicists Peter Hegemann, Georg Nagel and Ernst Bamberg in Germany, which showed that these proteins can generate electrical currents in animal cells, not just in algae.

Flicking the Switch

These studies inspired the team to insert Spudich's light-sensitive algal proteins into cultured neurons from rats and mice via a pioneering genetic engineering method that developed by the team. When exposed to light in laboratory tests in 2004, these inserted proteins generated electric currents — just as they did in the light-sensitive algae from which they originated. But instead of turning on light-chasing behaviors as they did in the algae, these currents — when generated in target neurons — turned on the normal electrochemical signaling of the neurons, as desired.

In other words, the team showed that by selectively inserting light-sensitive proteins into target neurons, they could impart these neurons with light sensitivity so that they would be activated by light. The team thereby developed the basics of optogenetics — which is defined by Deisseroth as "the combination of genetics and optics to control well-defined events within specific cells of living tissue."

The members of the team (either working together or in other teams) also developed tools to:

• Turn off target neurons and stop their electrochemical signaling by manipulating light-sensing proteins.
• Deliver light to target neurons in laboratory animals via a laser attached to a fiber cable implanted in the brain.
• Insert light-sensitive proteins into various types of neurons so that their functions could be identified.
• Control the functioning of any gene in the body. Such control supports studies of how gene expression in the brain may influence neurochemical signaling and how changes in key genes in neurons may influence factors such as learning and memory.

"The brain is a mystery, and in order to solve it, we need to develop a great variety of new technologies," says Boyden. "In the case of optogenetics, we turned to the diversity of the natural world to find tools for activating and silencing neurons — and found, serendipitously, molecules that were ready to use."

The Power of Optogenetics

Thousands of research groups around the world are currently incorporating increasingly advanced techniques in optogenetics into studies of the brains of laboratory animals. Such studies are designed to reveal how healthy brains learn and create memories and to identify the neuronal bases of brain diseases and disorders such as Parkinson's disease, anxiety, schizophrenia, depression, strokes, pain, post-traumatic stress syndrome, drug addiction, obsessive-compulsive disease, aggression and some forms of blindness.

Deisseroth says, "What excites neuroscientists about optogenetics is control over defined events within defined cell types at defined times — a level of precision that is most crucial to biological understanding even beyond neuroscience. And milliscale-scale timing precision within behaving mammals has been essential for key insights into both normal brain function and into clinical problems, such as parkinsonism."

Indeed, optogenetics is now so important to brain research that it is considered one of the critical tools for the Brain Research through Advancing Innovative Neurotechnologies through Advancing Innovative Neurotechnologies (BRAIN) Initiative, which was announced by President Obama in April 2013.

In addition, optogenetics is being applied to other organs besides the brain. For example, NSF-funded researchers are working to develop optogenetic techniques to treat cardiac arrhythmia.

The Laws of Unintended Consequences

As with many pivotal scientific advances, the development of optogenetics was built upon many basic-research studies that had been inspired by the intellectual curiosity of researchers who could not possibly have foreseen the important practical applications of their work. "The development of optogenetics is yet one more beautiful example of a revolutionary biotechnology growing out of purely basic research," says Spudich.

What's more, many of the varied disciplines that contributed to the invention of optogenetics — including electrical engineering, genetic engineering, physics and microbiology — may seem, on first blush, unrelated to one another and to brain science. But perhaps most surprising was the importance of basic research on algal proteins to the development of optogenetics.

Deisseroth said, "The story of optogenetics shows that hidden within the ground we have already traveled over or passed by, there may reside the essential tools, shouldered aside by modernity, that will allow us to map our way forward. Sometimes these neglected or archaic tools are those that are most needed--the old, the rare, the small and the weak."Food for thought for anyone tempted to dismiss the algae in a murky body of water as worthless pond scum!

Editor's Note: The researchers depicted in Behind the Scenes articles have been supported by the National Science Foundation, the federal agency charged with funding basic research and education across all fields of science and engineering. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author and do not necessarily reflect the views of the National Science Foundation. See the Behind the Scenes Archive.

Introduction

About 1 to 2 percent of the human population has red hair.

Redheads have genes to thank for their tresses. Research shows red hair usually results from a mutation in a gene called MC1R, which codes for the melanocortin-1 receptor. The pigment found in redhair that makes it red is called pheomelanin. 

But redheads as a group have more in common than only their hair color -- certain health conditions appear to be more common among people with red hair.

Here are five health risks linked with being a redhead.

More sensitive to pain

Redheads appear to be more sensitive to pain, and less sensitive to the kinds of local anesthesia used as the dentists, research recent suggests.

A 2004 study found that redheads required significantly more anesthetic in order to block pain from an unpleasant electric stimulation.

Another study found that redheads are more sensitive to sensations of cold and hot, and that the dental anesthetic lidocaine is less effective for redheads.

The MC!R gene that can cause red hair codes for a receptor that is related to a family of receptors involved in perceiving pain, which may explain why mutations in MC1R would increase pain perception.

Because of their increased pain sensitivity and reduced tolerance to anesthesia, redheads may avoid the dentist. A 2009 study found that redheads were more anxious about dental visits, had more fear that they would experience pain during a visit, and were more than twice as likely to avoid dental care than those without the MC1R gene. [See What Really Scares People: Top 10 Phobias]

Increased Parkinson's risk

A 2009 study of more than 130,000 people who were followed for 16 years found that those with lighter hair colors were at increased risk for Parkinson's disease compared to those with black hair.

Redheads had the highest risk — they were nearly twice as likely to develop Parkinson's, compared to people with black hair.

Skin cancer risk

Redheads often have fair skin, a trait known to increase skin cancer risk. In addition, the particular genetic mutation that leads to red hair may further boost the risk of skin cancer, recent research suggests.

A new study finds thatmutations in the MC1R gene — which cause red hair, fair skin and poor tanning ability — also set up skin cells for an increased risk of cancer upon exposure to ultraviolet (UV) radiation.

The mutation prevents MC1R from properly binding to a gene called PTEN, which helps protect against cellular changes that promote cancer. As a result, after exposure to UV rays, PTEN is destroyed at a higher rate, and growth of pigment producing cells (called melanocytes) is accelerated as it is in cancer, the researchers said.

Because the study was conducted on mice and cells in a lab dish, more research is needed to see if the same mechanism occurs in people.

Endometriosis risk

Some women with red hair may be at increased risk for endometriosis, a condition in which tissue from the uterus grows outside the uterus, often resulting in pain.

A 2006 study of more than 90,000 women ages 25 to 42 found that those who had red hair and were fertile were 30 percent more likely to develop endometriosis compared to women with any other hair color.

However, redheads who were infertile had a reduce risk of endometriosis compared to those of any other hair color.

Birthmarks

A 2012 study found children with rare birthmarks called Congenital Melanocytic Naevi were more likely to have the MC1R mutation that causes red hair than children without the birthmarks.

Congenital Melanocytic Naevi are brown or black birthmarks that can cover up to 80 percent of the body. About 1 in 20,000 children have large or multiple CMN.

Study researcher Dr. Veronica Kinsler, of Great Ormond Street Hospital in London, said: "If you have red hair in your family, these findings should not worry you, as changes in the red hair gene are common, but large CMN are very rare. So the changes do not cause the CMN to happen, but just increase the risk."

A rare sleep disorder that causes people to punch and kick others during sleep may have some of the same risk factors as Parkinson's disease, and could give researchers clues to predicting Parkinson's many years before it surfaces, a new study suggests.

The results revealed a number of factors linked with an increased risk of REM sleep behavior disorder (or RBD), including smoking, working on a farm, past head injuries and pesticide exposure.

A better understanding of how these factors might be at work in both REM sleep Behavior Disorder and Parkinson's could lead to a way of diagnosing Parkinson's and detecting it very early, said study author Dr. Ronald Postuma, a neurologist at McGill University in Montreal.

Patients with RBD typically make sounds or move during REM sleep. The condition has been linked with some forms of dementia and Parkinson's disease, with one study of 93 RBD patients showing that more than half developed a neurodegenerative disease over a 12-year period.

"People who have sleep problems who are otherwise healthy are at increased risk for developing Parkinson's and dementia," Postuma said. The findings are published online today (June 27) in the journal Neurology.

Violent sleep

Researchers surveyed 347 people in 10 countries with RBD about their lifestyles and other medical conditions, and compared the results to those of healthy people.

In order to tease out exactly what risk factors might connect Parkinson's to RBD, the researchers matched up the risk factors for RBD they found with factors known to affect people's risk of developing Parkinson's.

But while the study may shed some light on what might lead to RBD, it also further clouds the mystery of what causes Parkinson's, the researchers said.

For example, previous research has shown what appears to be smoking's protective effect when it comes to Parkinson's — tobacco users have a lower risk of developing the disease. However, tobacco users in this study were 43 percent more likely to develop RBD than nonusers.

Similarly, caffeine use has been linked with a lower risk of Parkinson's, but in the new study, it did not appear to have an effect on developing RBD.

Most people don't need to be particularly concerned with developing RBD, said Dr. Karin Wirdefeldt, a medical epidemiologist with the Karolinska Institute in Stockholm, who was not involved in the new study. "However, a general recommendation is to avoid exposures such as smoking and pesticides due to their potential harmful effects related to conditions other than RBD or [Parkinson's]."

The link between neurological diseases and sleep

One concern Wirdefeldt said about the research was that patients had to rely on their memories for the surveys, and this may mean that the actual increased risk of RBD linked with certain behaviors are likely to be lower.

"As the first study on the topic, it is considered exploratory," she said.

Wirdefeldt added that "10 years after RBD diagnosis, most patients have still not developed a neurodegenerative disease."

But Postuma said that it's for that reason that Parkinson's researchers should take a deeper look at sleep disorders.

"Sleep disorders can be the first sign of Parkinson's,10, 20 years before you get it," Postuma said.

Early diagnosis, he said, would ultimately help the patients who might develop these disorders.

Pass it on: A violent sleep disorder might be an early indicator of Parkinson's.

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NEW ORLEANS — A drug used to treat Parkinson's disease may also make people less impulsive, a new study suggests.

After taking the drug, study participants were better able to delay gratification — or quell their impulse for an immediate reward, and hold out for a larger one — compared with before they took the drug.

The researchers said the drug could be used to help people with disorders of impulse control, such as gambling, substance abuse or compulsive stealing, said study researcher Dr. Andrew Kayser, an assistant professor of neurology at the University of California, San Francisco.

However, the study was conducted in a laboratory, and the situations participants faced were hypothetical. Kayser and colleagues are now conducting research to see if the drug can reduce impulsiveness in real-world settings.  

The study will be presented here this week at the American Academy of Neurology annual meeting.

The study involved 25 healthy people, ages 19 to 41. Participants answered a series of questions in which they had to choose between receiving a small amount of money immediately, or a larger amount of money later on. (While participants did not actually receive the money, research has demonstrated that more impulsive people tend to pick the smaller, more immediate reward over the larger, delayed reward.)

After taking the drug, called tolcapone, participants chose the immediate reward less often than they did when they were not on the drug. The greatest reduction in impulsivity was seen in people who were the most impulsive, Kayser said.

People who are impulsive are thought to have less dopamine — a chemical responsible for signaling feelings of reward and pleasure — available in their brain. The drug works by inhibiting the breakdown of dopamine in the brain's prefrontal cortex, which is responsible for inhibiting impulsive behaviors. By increasing dopamine in this region, the drug is thought to improve a person's ability to control their behaviors, Kayser said.

Unlike stimulants, which are sometimes used to improve attention and reduce impulsive behaviors, tolcapone does not produce a high, meaning it may have less potential for abuse, Kayser said.

However, people who take tolcapone need to be monitored to make sure the drug does not affect their liver function, and consuming alcohol with the drug can be dangerous, Kayser said.

Pass it on: A drug may be able to reduce impulsivity and help people with problems such as substance abuse and gambling.

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A colonoscopy or similar test could one day diagnose Parkinson's disease years before symptoms occur. That's because signs of Parkinson's that appear in the brain also show up in the colon, a new study says.

Researchers examined tissue samples obtained during colon exams of people who later developed Parkinson's disease. The samples were taken several years before the patients showed symptoms of the neurological disorder.

The cells in the patients' intestinal walls were found to contain clumps of alpha-synuclein — a hallmark protein of Parkinson's.

In a previous study, these researchers found these aggregates were apparently unique to the gut of Parkinson's disease patients — they were not seen in people with certain gut disorders or in healthy people.

The findings suggest that tissue obtained during a colonoscopy or other colon cancer screening test could one day be used to predict who will develop Parkinson's, said study researcher Dr. Kathleen Shannon, a neurologist at Rush University Medical Center in Chicago.

However, first the findings will need to be replicated in studies that include more people, including people with other types of brain diseases, the researchers said.

Currently doctors cannot diagnose Parkinson's until patients show symptoms, such as shaking, slowed movements and stiff muscles. By then, however, the patients' brains have deteriorated significantly. Finding early markers of the disease could lead to a way to slow or stop the progression, the researchers said.

Predicting Parkinson's

Parkinson's disease is caused by loss of brain cells that produce dopamine, a brain chemical needed to control muscle movement. One change that occurs in the brains of Parkinson's patients is the formation of clumps called Lewy bodies. The protein alpha-synuclein is found in all Lewy bodies, according to the Mayo Clinic.

Recent research suggests the Parkinson's disease process begins in nerve cells in the gut and spreads to nerves in the brain, Shannon said.

In a 2011 study, Shannon and colleagues examined intestinal tissue samples taken from nine Parkinson's patients, 23 healthy people and 23 people with Crohn’s disease or ulcerative colitis (both types of inflammatory bowel disease). The people in the study ranged in age from early 20s to late 70s.

All nine Parkinson's disease patients had clumps of alpha-synuclein in the nerves of their gut tissue, while none of the healthy people or people with gut disorders did. Two healthy people and three colitis patients had a small amount of alpha-synuclein in their cells, but it was distinct from the amount seen in the Parkinson's patients.

In a study published today (May 15) in the journal Movement Disorders, the researchers reported they examined tissue samples from three patients taken during colonoscopies two to five years before the patients developed Parkinson's disease symptoms. All the patients had the characteristic aggregates of alpha-synuclein in their gut.

Provoactive study

"It's really interesting and provocative," Dr. William Weiner, a neurologist at the University of Maryland School of Medicine and member of the American Academy of Neurology, said of the study findings. The hypothesis that Parkinson's disease starts in the gut has not had much tangible evidence until now, Weiner said.

However, the new study does not demonstrate that clumps of alpha-synuclein in the gut develop before the protein begins to show up in the brain, Weiner said.

"The same changes might be going on in the brain at the same time," he said.

The idea that alpha-synuclein forms deposits in tissues other than the brain in Parkinson's patients is pretty well established, said Dr. Kenneth Marek, president and senior scientist at the Institute for Neurodegenerative Disorders, a research company in New Haven, Conn. However, "to what extent these findings suggest where the disease might begin or how it might begin is a much murkily question," Marek said.

But Marek agreed the findings suggest tissue samples taken during a colonoscopy "could be helpful in understanding whether you are at high risk to develop Parkinson's," Marek said.

Because the new study looked at only three people, much larger studies are needed to confirm the findings, Weiner said.

Pass it on:  A colonoscopy someday may be able to identify Parkinson's disease, but much more work is needed first.

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One of the highest-achieving athletes of the 20th century is boxing champion Muhammad Ali, but to Maryum Ali, he's just dad.

As she has watched her father become one of the most famous faces of Parkinson's disease since his diagnosis nearly 30 years ago, she has learned much about the realities of Parkinson's, said Maryum. who is known to her family as May May.

Currently, about 1 million people in the U.S. have Parkinson's, which results from a loss of the brain cells that produce the chemical dopamine. The condition causes tremors, rigid muscles and impaired balance.

In the early days of her father's diagnosis, information about the condition was scarce. "Even doctors didn’t understand it," she told MyHealthNewsDaily.

But still today, myths about Parkinson's persist.

"People think that it's a disease of older people," she said. While it's true that the majority of people with Parkinson's develop the condition around the age of 60, it is increasingly being diagnosed in younger people, she said.

About 10 percent of people with Parkinson's are diagnosed before age 40, according to the National Parkinson Foundation.

Another myth, Ali said, is that there is not much that can be done to help a person with Parkinson's. "There's this, 'it is what it is' mindset out there," she said.

People should know that there are effective ways to deal with the symptoms of Parkinson's, she said. Exercise enormously helped her father, she said.

In fact, a study published this month in the journal Geriatrics and Gerontology International found that of Parkinson's patients who participated in weekly, one-hour exercise sessions reported improvements in their daily activities compared with a control group who didn’t exercise.

Brain stimulation treatments also help, Ali said. It's important to find a specialist who is familiar with all available options, she said. "You can do lots of different things; it's not like there's no hope."

A third myth about the condition is that it's highly genetic, Ali said. "Lots of people think this, but only 5 percent of people who get it have a genetic tie," she said.

Scientists don’t know exactly what causes Parkinson's disease. While genetics play a role, most researchers believe that chemicals in the environment increase a person's risk of the condition, according to the National Institutes of Health.

Viruses and inflammation in the body have also been linked with the condition, the NIH says.

Pass it on: Parkinson's disease can strike younger people, but for all patients, exercise and other treatment may help with symptoms.

Follow Karen Rowan @karenjrowan. Follow MyHealthNewsDaily @MyHealth_MHND, Facebook & Google+. Originally published on MyHealthNewsDaily.

Compounds called flavonoids, found in berries, tea and red wine, may reduce men's risk of Parkinson's disease, a new study suggests.

Men in the study who consumed high amounts of flavonoid-rich foods were 40 percent less likely to develop Parkinson's disease over a 20-year period than those who consumed low amounts of these foods.

The findings add to the growing body of evidence suggesting that regular consumption of some flavonoids can have a marked effect on human health, said study researcher Aedin Cassidy, professor of diet and health at the University of East Anglia in the United Kingdom. Studies suggest these compounds may offer protection against diseases such as heart disease, high blood pressure, some cancers and dementia.

The study found an association, not a direct cause-effect link. More research is needed to determine exactly how big an impact diet has on the development of Parkinson's disease, Dr. Kieran Breen, director of research at the charity Parkinson's UK, said in statement.

The study involved about 130,000 men and women who were followed for 20 to 22 years. Every four years, participants were given a survey that asked how frequently they ate certain foods. More than 800 participants developed Parkinson's disease during the study period.

No link was found between overall consumption of flavonoids and Parkinson's disease risk in women.

But a link was found for both genders between Parkinson's risk and consumption of a subgroup of flavonoids called anthocyanins, which are found in berries.

Participants who ate one or more servings of berry fruits each week were around 25 percent less likely to develop Parkinson's disease than those who did not eat berry fruits. Strawberries and blueberries were the top two sources of anthocyanins.

Anthocyanins, may be particularly beneficial for the brain, Cassidy said.

The study was published today (April 4) in the journal Neurology. A preliminary version of the study was presented last year at the American Academy of Neurology's annual meeting.

Pass it on: Regular consumption of berries and other foods rich in flavonoids may reduce the risk of Parkinson's disease, particularly in men.

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Some personality traits appear to be linked with the risk of developing Parkinson's disease, a new study suggests.

The results show patients with Parkinson's disease are more likely to be cautious and avoid taking risks compared with people who don't have Parkinson's.

Moreover, the tendency to avoid taking risks appears to be a stable personality trait across a patient's lifetime — as far back as 30 years before symptoms began, those with Parkinson's disease said they did not often engage in risky or exhilarating activities, such as riding roller coasters or speeding, the study found.

The findings add to a growing body of research suggesting Parkinson's is more likely to afflict people with rigid, cautious personalities.

It's possible that what we consider to be aspects of someone's personality may in fact be very early manifestations of Parkinson's, said study researcher Kelly Sullivan, of the University of South Florida's department of neurology. However, much more research is needed to confirm this hypothesis, Sullivan said.

It's also way too soon to say that having a "look before you leap" personality puts you at risk for Parkinson's.

"I'm not a big risk-taker, but at the same time, I haven't resigned myself that I'm going to have Parkinson's," Sullivan said.

Parkinson's personality

Since the early 1900s, there have been reports that Parkinson's patients tend to be industrious, punctual, cautious and risk-averse. Most studies that have found a link between Parkinson's and a risk- avoidant personality have been based on assessments of patients' personalities prior to the disease, using questions such as "did you take risks when you were younger?" However, remembering what you were like many years ago may be difficult, and what someone considers a "risk" is subjective, Sullivan said.

In the new study, Sullivan and colleagues asked 89 patients with Parkinson's and 99 healthy people whether they engaged in specific activities— such as riding roller coasters, speeding and wearing a seatbelt— before the age of 35.

They also asked questions to gauge participants' current personalities.

The results showed that participants with Parkinson's had higher levels of neuroticism — a personality trait associated with experiencing more negative emotions such as anxiety — and higher levels of harm-avoidance compared with healthy participants. In general, participants' willingness to take risks tended to be stable over time, and Parkinson's patients tended to report they took fewer risks.

Another study by Sullivan and colleagues found women with Parkinson's disease were 60 percent more likely to say they had a routine lifestyle as a young adult (such as getting up and going to bed at the same time every day) compared with people without Parkinson's.

Too little dopamine

A brain chemical called dopamine is needed to control muscle movement, and in Parkinson's disease patients, the brain cells that produce dopamine start to die. This cellular death leads to the tremors and difficulty with walking, movement and coordination, which are hallmarks of Parkinson's.

Levels of dopamine may also affect personality. Dopamine is responsible for signaling feelings of reward and pleasure. "When you take a risk or jump out of an airplane, that’s what gives you that reward feeling," Sullivan said.

"If you have lower levels of dopamine, it's less likely that you would really get that neurochemical reward and say 'That was awesome! Let's keep doing that,'" Sullivan said.

While the symptoms of Parkinson's don't show up until about 70 percent of dopamine-producing cells have deteriorated, Sullivan said, it's possible the loss of dopamine-producing cells goes on for a long period before someone is diagnosed, Sullivan said.

More research is needed to know exactly how long this process of brain cell loss goes on, and whether the risk-avoidant behaviors exhibited early in life by Parkinson's patients are actually manifestations of the disease, Sullivan said.

Sullivan's studies were presented last week at the American Academy of Neurology meeting in New Orleans.

Pass it on: Parkinson's diseases patients tend to have more cautious personalities.

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Taking statins may lower the risk of developing Parkinson's disease, particularly among people younger than 60, a new study suggests.

Overall, people who took cholesterol-lowering statins had a 26 percent decreased risk of developing Parkinson's disease over a 12-year period. For those under 60, the risk was reduced by 69 percent.

The results held even after the researchers took into account other factors that may heighten the risk of Parkinson's disease, such as smoking.

However, the results should be interpreted with caution, the researchers said. For starters, the calculations they made to determine whether their findings could be due to chance, instead of a real risk-reducing effect, showed that the results met this criteria, but just barely.

In addition, about 30 percent of people categorized as taking statins were likely taking another type of cholesterol-lowering drug.

In addition, statins have been found to lower blood levels of coenzyme Q, a substance that may protect against Parkinson's disease and is actually being tested as a treatment for the condition.

Because of this, and other potentially adverse effects of statins, more studies are needed to clarify the effect of these drugs on Parkinson's disease, including whether only certain types of statins have a beneficial effect.

Previous studies on whether statins reduce the risk of Parkinson's disease have had mixed results, although a 2005 study found that the drugs do not worsen the disease.

In the new study, researchers from Brigham and Women's Hospital and Harvard School of Public Health in Boston followed 38,000 men and 91,000 women from 1994 to 2006. Participants were periodically asked whether they were taking statins.

During the study period, 644 cases of Parkinson's disease occurred: 593 among the 118,031 people who did not take statins (or 0.5 percent), and 51 among the 11,035 people who did take statins (or 0.46 percent).

For those over 60, there was no link between statin use and a lower risk of Parkinson's disease.

Statins might lower the risk of Parkinson's because they reduce inflammation in the brain, the researchers said.

Among the study's limitations are that it did not take into account the drugs' potencies, doses or abilities to cross into the brain, said Dr. Fatta Nahab, an assistant professor of neurology and neuroscience at the University of Miami Miller School of Medicine, who was not involved in the study.

"Since the brain changes associated with Parkinson disease occur over years to decades, it will also be challenging to design clinical trials to observe the modest differences identified in this study," Nahab said.

The study is published in the March issue of the journal Archives of Neurology. One of the study researchers served as a consultant for Teva Pharmaceuticals, which manufactures a statin. The study was funded by the National Institutes of Health and the National Institute of Neurological Disorders and Stroke.

Pass it on:  Use of statins may lead to a moderate reduction in the risk of Parkinson's disease, but more research is needed to confirm the link.

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When we come down with the flu, we might think the worst is over after a week of a sore throat and body aches. But such viral infections may have lasting, unseen effects on the brain, emerging research suggests.

Viruses such as influenza and herpes may leave brain cells vulnerable to degeneration later in life, and increase the risk of developing diseases such as Alzheimer's and Parkinson's, research suggests. That's because these the viruses can enter the brain and trigger an immune response — inflammation — which can damage brain cells.

Viruses and other sources of inflammation "may be initiating factors in some of the most common neurological diseases," said Dr. Ole Isacson, professor of neurology at Harvard Medical School, who discussed the topic in an article published today (Feb. 15) in the journal Science Translational Medicine.

It's unlikely one bout of the flu will cause significant damage. But over a lifetime, injuries to cells accumulate, Isacson said, and along with environmental stresses, this can kill cells and the development of brain diseases. Variations in the number of infections we get may be the difference between a person developing Parkinson's disease at age 65 or at age 95, Isacson said.

It's possible that toning down the inflammation that occurs shortly after viral infection could reduce cell damage and the risk of subsequent brain disease, Isacson said. Isacson pointed to a 2011 study of 135,000 men and women found that those who took ibuprofen (a medication that can reduce inflammation) were 30 percent less likely to develop Parkinson's over a six year period compared to those who did not take the medication.

Brain infection

One of the earliest pieces of evidence for the virus-brain disease link comes from the 1918 influenza pandemic, according to Isacson's article. After that outbreak, there was a dramatic increase in cases of a disease called postencephalitic parkinsonism, which has many of the same symptoms as Parkinson's.

In a more rigorous test of the link, a 2009 study showed that mice injected with the H5N1 flu virus developed infections in cells in a brain region known to be significantly impacted by Parkinson's disease, Isacson said.

Research has also shown that infection with certain herpes viruses can increase the risk of Alzheimer's disease. And very rarely, encephalitis, or brain inflammation caused by viruses, can lead directly to an acute, but transient, form of Parkinson's disease.

But more often, viral infections in our brain are silent, Isacson said. We don't see the full impact of these infections until brain degeneration is substantial, he said.

Preventing disease

Several weeks after infection, inflammatory molecules known as cytokines reach a peak concentration, Isacson said. It's this "cytokine storm" that Isacson and his colleagues suspect is responsible for the brain cell damage associated with viral infections.

If researchers could find a way to block this peak from occurring, they might reduce the risk of certain neurological diseases, Isacson said.

In addition, researchers could also try to identify viruses that cause particularly severe cytokine storms, to better understand which infections pose the greatest risk to the brain, Isacson said.

The idea that immune system inflammation may influence the development of Alzheimer's disease and other neurological disorders is just one hypothesis out of many that are being investigated today, said Heather Snyder, senior associate director of medical and scientific relations at the Alzheimer's Association. More research is needed to understand what, if any, effect the immune system has on brain diseases, Snyder said.

Pass it on: Infection with certain viruses may increase the risk of brain diseases.

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Lovers of red wine rejoiced when it was found to contain resveratrol — a compound purported to increase health and maybe even lengthen life. But studies have suggested that to see benefits, you would need to consume large amounts of the compound — more than is found in a bottle of wine.

Now a new study suggests we could get the equivalent of large resveratrol doses from pills we already have— a class of drugs that are being tested for use as treatments for Alzheimer's and Parkinson's disease.

The findings suggest these drugs, known as known as phosphodiesterase type 4 (PDE4) inhibitors, may provide a practical way to reap red wine's benefits than consuming buckets of the stuff (which would certainly carry health risks).

"[The study] reveals a novel utility for this class of drugs that hasn’t been explored before," said study researcher Dr. Jay H. Chung, chief of the Laboratory of Obesity and Aging Research at the National Heart, Lung, and Blood Institute.

However, the study was conducted in mice, and the results will need to be replicated in people.

Why red wine is healthy

In the study, scientists aimed to figure out exactly how resveratrol, a compound in red wine, acts inside cells. They discovered resveratrol works in a different manner than previously thought.

The study showed that resveratrol inhibits a protein known as phosphodiesterase type 4 (PDE4).That meant that resveratrol is a PDE4 inhibitor.

Knowing that drugs called PDE4 inhibitors werebeing tested to treat Alzheimer's, the researchers gave one such drug, called rolipram, to mice.

They found the drug produced all the health benefits of resveratrol, including preventing diet-induced obesity and improving control over blood sugar levels.

In studies on people, resveratrol has been shown to have anti-diabetes effects. But people would need to consume about 1,000 bottles of red wine a day in order to take in enough resveratrol to see true health benefits, Chung said.

PDE4 inhibitors could provide a realistic way for people to get the same benefits, the researchers said. In addition, PDE4 inhibitors may be less toxic than resveratrol itself, because the compound interacts with many proteins inside cells.

"By just targeting the key player [PDE4] you minimize the potential for adverse effects," Chung said.

Chung said he is planning to conduct a follow-up study that examines the effects of rolipram on obese people with insulin resistant.

Another PDE4 inhibitor, called roflumilast, is already approved as a treatment for people with chronic obstructive pulmonary disease (COPD). The side effects of this drug include diarrhea, nausea and dizziness, according to the National Institutes of Health.

Treating diseases

"I think this is a huge step forward in the understanding of what resveratrolcan do at the biological level," said Philippe Marambaud, an Alzheimer's researcher at the Feinstein Institute for Medical Research in Manhasset, N.Y., who has researched resveratrol and was not involved in the new study.

By finding out how resveratrol works, the study helps researchers who are investigating whether the compound can have therapeutic effects for other diseases, such as Alzheimer's disease, Marambaud said.

However, future studies will need to replicate the findings to be sure that resveratrol does indeed inhibit PDE4, Marambaud said.

In addition, although the study suggests PDE4 inhibitors can mimic resveratrol,. researchers should continue investigating the effects of resveratrol, as well as those of PDE4 inhibitors. "You don't want to think that one approach will work better than another," Marambaud said.

The new study will be published Feb. 3 in the journal Cell.

Pass it on: A class of drugs called PDE4 inhibitors mimic the effect of resveratrol.

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Inserting a particular gene into the brains of patients with Parkinson's disease could reduce symptoms of the disease, including tremors, and also improve patients' ability to move, according to a new study.

The work is the first rigorously designed study to show that this technique, known as gene therapy, can be effective for people with Parkinson's disease, or any neurological disease for that matter. Patients who received the gene therapy showed greater benefits than those who received a placebo. Both groups of patients underwent brain surgery, but only one group received gene therapy.

The treatment is intended for a subgroup of Parkinson's patients — those who do not respond to medication very well. Of the 1 million to 1.5 million Americans with Parkinson's, about 10 to 15 percent of them, or 100,000 to 200,000 people, fit into this category, said study researcher Dr. Michael Kaplitt, vice chairman for research in the Department of Neurological Surgery at Weill Cornell Medical College in New York.

The study "brings us much closer to having a gene therapy that might be ready for general use," Kaplitt said. The work paves the way for gene therapies for other types of brain diseases, he said. "I think we are now helping to facilitate and to accelerate the development of a whole host of gene therapies … for diseases such as Alzheimer's disease, epilepsy [and] depression," he said.

Others argue that the effect, while real, is minimal.

"It's important that there was a change, but it was a very small change," said Dr. William Weiner, a professor of neurology at the University of Maryland Medical Center, who studies Parkinson's disease and was not involved in the study. The idea that inserting a single gene is the answer for neurodegenerative diseases is probably simplistic, Weiner added.  He also notes that gene therapy does not cure the disease, it only treats the symptoms.

The findings still need to be confirmed in a larger group of patients, since this study involved just 22 individuals, and it remains to be seen how long the benefits last.

Gene therapy

In those with Parkinson's disease, brain cells deteriorate in an area of the brain that controls muscle movement. Symptoms can include tremors, stiffness in the arms and legs, and trouble with coordination, according to the National Institutes of Health.

In these patients, the levels of a brain chemical called GABA are substantially reduced, Kaplitt said. This chemical is "used to quiet down neurons when they're firing excessively," Kaplitt said. Reductions in GABA cause problems in the parts of the brain responsible for coordinating movement, he said.

In the trial, 22 Parkinson's patients had a gene inserted in their brains to produce more GABA. The gene is delivered into cells with the help of a virus. Twenty-three patients received the placebo.

The researchers rated the patients' symptoms, including the severity of tremors and stiffness, and came up with a single "motor score" that represented how well they could move.

Six months after the surgery, patients given the gene therapy had a 2.1 percent improvement on their motor scores on average, while patients in the placebo group had a 12.7 percent improvement on their scores.

Treating more patients

Patients in this study also would be candidates for deep brain stimulation, another surgical treatment for Parkinson's disease. But gene therapy has several advantages over deep brain stimulation. For instance, gene therapy requires only one surgery, while deep brain stimulation requires multiple surgeries to maintain the hardware (a nerve control device) involved.

Only a small portion of those eligible for deep brain stimulation actually receive it, for various reasons, including the cost and long-term upkeep, Kaplitt said.

"We believe we may be able to expand that pool of patients that would be good candidates for surgical interventions," he said.

The study appears today (March 17) in the journal Lancet Neurology.

Pass it on: Gene therapy can improve symptoms in Parkinson's disease patients. The effects, while real, are quite small, experts say.

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Weekly use of ibuprofen may decrease your risk of developing Parkinson's disease, a new study suggests.

People who took ibuprofen at least twice a week were 38 percent less likely to develop Parkinson's disease over the six-year study than people who didn't take the painkiller, said study researcher Dr. Xiang Gao, a researcher at the Harvard School of Public Health in Boston.

"This could be due to some unique effects of ibuprofen on [the central nervous system]," Gao told MyHealthNewsDaily.

But people should not start taking ibuprofen only to reduce their Parkinson's disease risk, because health risks come with long-term use of the drug, Gao said. And more research is needed to determine if its use is the direct cause of the decreased Parkinson's risk, or if other factors are at play, he said.

The study was published online today (March 2) in the journal Neurology.

Ibuprofen association

Gao and his colleagues studied data from more than 136,000 people. The participants also reported their use of ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs).

At the end of the six-year period, 291 people had been diagnosed with Parkinson's disease.

Those who took ibuprofen at least twice a week were 38 percent less likely to develop Parkinson's than people who didn't take it, the study said.

And when the findings are combined with the results of other studies, it emerges that people who take ibuprofen have a 27 percent lower risk of developing Parkinson's disease, compared with people who don't take the drug, Gao said.

Looking at the causes

The exact cause of Parkinson's disease, which is characterized by muscle tremors and difficulty walking and moving, is unknown. Past studies suggest it is associated with the absence of the chemical messenger dopamine, as well as damage to the nerve endings that make the neurotransmitter norepinephrine, according to the Mayo Clinic.

It could be that ibuprofen protects against Parkinson's disease by stopping inflammation that spurs the loss of dopamine, the study said.

While the study convincingly showed that ibuprofen use is associated with a decreased risk in Parkinson's, a causal relationship still has yet to be demonstrated, said Dr. James H. Bower, of the Mayo Clinic in Rochester, Minn., who wrote an editorial about the study.

"One explanation for the association that they found is what everyone would like to believe: that it actually is protective," Bower told MyHealthNewsDaily. "That'd be great, and that's a possibility, but there are other possibilities that could also explain the association."

For example, people who have gastrointestinal problems tend to have a greater risk of Parkinson's disease than people with healthy digestive systems, Bower said. And those same people may also shy away from taking ibuprofen because the drug is known to increase the risk of such problems, including internal bleeding and kidney failure, he said.

Or, hypothetically, there may be a gene that protects people from Parkinson's disease that's located right next to another gene that makes people more likely to have osteoarthritis, Bower said.

So people who develop osteoarthritis may take a lot of ibuprofen to relieve the arthritis pain. But that ibuprofen intake wouldn't actually be related to Parkinson's risk, he said.

It's also hard to pinpoint any one factor that decreases Parkinson's disease risk because the disease develops over such a long period of time, Bower said.

The side effects of long-term use of ibuprofen still outweigh the potential benefits of the drug in preventing Parkinson's, Bower said. But if the study’s findings are replicated in future research, ibuprofen-like drugs (without the side effects) could be a promising preventive treatment for Parkinson's disease, he said.

Pass it on: Weekly ibuprofen use is associated with a decreased risk of developing Parkinson's disease.

Follow MyHealthNewsDaily staff writer Amanda Chan on Twitter @AmandaLChan.

This story was provided by MyHealthNewsDaily, a sister site to LiveScience.

This Behind the Scenes article was provided to LiveScience in partnership with the National Science Foundation.

Basiru Leigh peers into a microscope in the lab of Oliver Hobert of Columbia University in NY. Leigh is examining mutant ground worms from a species known as C. elegans.

"There! You see?" he exclaimed. "They are moving abnormally — in a circle instead of a U-shape." This uncoordinated movement is a symptom of the worms' motor neuron disease; Leigh is trying to find the cause. His hypothesis: two transcription factors, proteins that regulate the expression of other genes, play a role in the mutant worms' abnormal movements. 

Some of the most vexing and horrific human diseases, such as Spinal Muscular Atrophy and Amyotrophic Lateral Sclerosis, are neurological disorders that result from the degeneration and death of motor neurons, the cells that control muscle activity like speaking, walking, breathing and swallowing. 

Understanding the root causes of these diseases would be one benefit of the research taking place in Hobert's lab at Columbia. Under Hobert's guidance, post-docs and graduate students — and a handful of younger students like Leigh — are trying to figure out how neurons develop and differentiate in C. elegans, a microscopic worm whose nervous system is analogous in many ways to that of humans. 

Leigh has the opportunity to work in Hobert's lab thanks to Harlem Children Society, an NSF-funded program created ten years ago by Sat Bhattacharya, a molecular geneticist at Memorial Sloan Kettering. 

The goal of the non-profit is to encourage low-income and minority high school students (95 percent minority; more than 58 percent female) to pursue careers in science, technology, engineering, and math (STEM) and allied disciplines through a unique, hands-on program that includes paid research internships at leading institutions and weekly workshops and seminars. 

Harlem Children Society began in New York City, but has expanded and customized its program to meet local needs at rural and urban sites across the United States and the globe. 

Leigh began with Harlem Children Society five years ago, when he was 15 years old and entering his sophomore year at the Bronx High School for Medical Science. He credits the program with his success at City College, where he just completed his second year with a double major in biology and computer science. 

This summer, Leigh is one of two Harlem Children Society students working in Hobert's lab. Leigh is working under the direct mentorship of Paschalis Kratsios, a post-doc whose research focuses on the role of several transcription factors in motor neuron development and survival. Transcription factors are critical because of their role regulating the expression of so many other genes. An understanding of how they work could allow scientists to control the process of neuron development and ultimately find treatments for neurological diseases like Parkinson's, Alzheimer's and Amyotrophic Lateral Sclerosis.

Kratsios has designed a simple but important project that Leigh can complete during the 12-week duration of his mentorship: a study of transcription factors Vab-15 and Zag-1 and their role in coordinating the movements of C. elegans. 

C. elegans is a particularly useful organism for neurological research because it has a simple nervous system (a total of 312 neurons) and a three-day developmental cycle. It also has transparent skin, which is helpful when examining motor neurons under a microscope.

Leigh began his research looking at the role of Transcription Factor Zag-1 using a basic genetic experiment. First, he bred genetically normal worms, whose motor neurons were marked with green florescent proteins (GFPs), with mutant worms missing Zag-1. Then Leigh separated out the progeny demonstrating the same uncoordinated movements as their mutant parents. The progeny's motor neurons were now all marked with GFPs and, using a florescent microscope, Leigh was able to count them to find out if the uncoordinated progeny had fewer motor neurons than their normal parents. 

Leigh's finding was surprising: the uncoordinated offspring did have all their motor neurons. Leigh was now able to conclude that the absence of Zag-1 does not affect the survival of motor neurons. The uncoordinated movements of the mutant worms could instead result from some or all of the motor neurons not working correctly. But in exactly what way are they dysfunctional? This question is what Leigh hopes to answer in the next phase of his research.

To answer it, Leigh will conduct another genetic experiment. This time he will breed Zag-1 mutant worms with normal worms bearing GFPs activated only when motor neurons release their neurotransmitters. Leigh expects that when he examines the uncoordinated progeny of this new pairing, some of their motor neurons will not light up with GFP. This result would indicate that the absence of Zag-1 affects the neurotransmitter pathway in C. elegans' motor neurons. 

Leigh said the experience of working with a mentor in a real lab is invaluable: "Dr. Kratsios explains everything in detail — I have learned so much more about genetics here than in class." And he is thrilled to have the opportunity to conduct his own research: "At my age, to get this chance to do my own research…it's the best." 

But for Leigh, who hopes one day to be a neurosurgeon, the most exciting thing about the experience is participating in research that might one day contribute to treatments for diseases like Parkinson's. "Muhammad Ali is one of my heroes," Leigh said, "so it's really cool to do something that could one day help him."

Editor's Note: This research was supported by the National Science Foundation (NSF), the federal agency charged with funding basic research and education across all fields of science and engineering.  Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author and do not necessarily reflect the views of the National Science Foundation. See the Behind the Scenes Archive.

A rare sleep disorder in which people act out their dreams, sometimes with violent thrashes, kicks and screams, may be an early sign of brain disorders down the line, including Parkinson's disease and dementia, a new study suggests.

The results suggest the incipient stages of these neurodegenerative disorders might begin decades before a person, or doctor, knows it, according to the researchers, who detail their findings online July 28 in the journal Neurology.

The researchers examined Mayo Clinic medical records to identify cases of the so-called REM sleep behavior disorder reported from 2002 to 2006. The researchers identified 27 patients who developed the REM sleep behavior disorder at least 15 years before showing symptoms of neurodegenerative ailments.

Of these patients, 13 developed what was likely dementia and mild cognitive impairment, 12 developed Parkinson's disease, one person Parkinson's-dementia, and one person multiple system atrophy (a disorder that causes symptoms similar to Parkinson's). The dementia category included dementia with Lewy bodies, which is the most common form of progressive dementia, defined partly by recurrent visual hallucinations.

Results showed the time between the start of the sleep disorder and the symptoms of the neurologic disorders ranged up to 50 years.

Scientists have estimated the REM sleep disorder has an estimated prevalence in adults of 0.4 percent to 0.5 percent and predominantly affects older adults. The main symptom of REM sleep behavior disorder is dream-enacting behavior, which can end in the person injuring themselves or a bed mate. When the person awakes, he or she might vividly recall the dream corresponding to the kicking or thrashing around. Past research has suggested a link between the dream-enacting behaviors and certain neurodegenerative ailments.

"A long-duration preclinical phase has important implications for epidemiologic studies and future interventions designed to slow or halt the neurodegenerative process," the researchers conclude.

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Higher levels of vitamin D appear to reduce the risk of an individual developing Parkinson's disease, a new report suggests.

Vitamin D is well known to play a role in bone health with emerging evidence suggesting a beneficial effect for lowering the risk of cancer, heart disease and type 2 diabetes.

"Recently, chronically inadequate vitamin D intake was proposed to play a significant role in the pathogenesis of Parkinson's disease," the authors write.

"According to the suggested biological mechanism, Parkinson's disease may be caused by a continuously inadequate vitamin D status leading to a chronic loss of dopaminergic neurons in the brain."

Individuals with higher levels of vitamin D appear to have a reduced risk of developing Parkinson's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.

Paul Knekt, D.P.H., and colleagues at the National Institute for Health and Welfare, Helsinki, Finland, studied 3,173 Finnish men and women age 50 to 79 who did not have Parkinson's disease at the beginning of the study, in 1978 to 1980.

Participants completed questionnaires and interviews about socioeconomic and health background, underwent baseline examinations and provided blood samples for vitamin D analysis.

Over a 29-year follow-up, through 2007, 50 of the participants developed Parkinson's disease. After adjusting for potentially related factors, including physical activity and body mass index, individuals in the highest quartile (one-fourth of the study population) of serum vitamin D levels had a 67-percent lower risk of developing Parkinson's disease than those in the lowest quartile of vitamin D levels.

"Despite the overall low vitamin D levels in the study population, a dose-response relationship was found," the authors write.

"This study was carried out in Finland, an area with restricted sunlight exposure, and is thus based on a population with a continuously low vitamin D status. Accordingly, the mean (average) serum vitamin D level in the present population was about 50 percent of the suggested optimal level (75 to 80 nanomoles per liter)"

The authors added, "Our findings are thus consistent with the hypothesis that chronic inadequacy of vitamin D is a risk factor for Parkinson's disease."

The exact mechanisms by which vitamin D levels may affect Parkinson's disease risk are unknown, but the nutrient has been shown to exert a protective effect on the brain through antioxidant activities, regulation of calcium levels, detoxification, modulation of the immune system and enhanced conduction of electricity through neurons, the authors note.