Drugs That Fight Herpes May Thwart Alzheimer's Disease

(Image credit: Skypixel | Dreamstime)

Antiviral drugs used to combat herpes virus infections could slow the progression of Alzheimer's disease, a new study suggests.

The herpes simplex virus type 1 (HSV1), which causes most cold sores , has previously been tied to the development of Alzheimer's disease.

In the study, cells infected with HSV1 showed a buildup of the proteins known to damage the brains of people with Alzheimer's. Treating the cells with the antiviral drug acyclovir significantly reduced the accumulation of these proteins.

The results are preliminary and future studies would need to determine if antiviral drugs can benefit Alzheimer's patients. And even if the treatment works, it is unlikely to be a cure, said study researcher Ruth Itzhaki, a professor at the University of Manchester in the United Kingdom. But, it could prevent the disease from causing extensive damage in the brain, Itzhaki said.

"If people could be treated at an early stage, [then] hopefully they might stay at that stage and not deteriorate further," Itzhaki said.

Herpes and Alzheimer's

More than 80 percent of Americans are infected with the herpes simplex virus (not everyone who is infected has symptoms).

Having HSV1 in the brain has been shown to be a risk factor for Alzheimer's disease in people with certain genetic mutations. And Itzhaki and colleagues previously showed that the genetic material of HSV1 is found within plaques present in the brains of Alzheimer's disease patients. These plaques, formed from accumulation of proteins called amyloid-beta , are a hallmark of the condition.

Itzhaki and colleagues infected cells in lab dishes with HSV1. They found the infection lead to buildup of amyloid-beta and tau another protein implicated in Alzheimer's disease.

After treatment with acyclovir, the tau protein was eliminated almost completely, andaccumulation of the amyloid-beta protein was reduced by 72 percent, compared with untreated cells.

Acyclovir has few side effects, Itzhaki said. The drug targets only the virus, and doesn't affect the normal functions of human cells, she said.

What about people?

The idea that the herpes virus causes Alzheimer's-related damage in human brains, and not just cells in a dish, is controversial.

"We need to see this work replicated and confirmed in other labs by independent teams of researchers," said William Thies, chief medical and scientific officer at the Alzheimer's Association. "There is no new insight in this [study] regarding the value in humans of this potential avenue of therapy," Thies said.

However, studies are increasingly showing a link between Alzheimer's and the herpes virus, said Dr. Elaine Bearer, a pathologist at the University of New Mexico School of Medicine.

"We've thought of [herpes virus] as a nuisance. It's probably not just a nuisance," Bearer said. One of Bearer's studies recently found that the herpes virus interacts with a protein that goes on to form amyloid-beta.

Because antiviral drugs against herpes are relatively safe and inexpensive, the fact that no studies have tested these drugs on Alzheimer's patients is "pretty crazy," Bearer said.

Both Bearer and Itzhaki said they hope to start trials in humans.

More research needs to be done to determine which antiviral drug or combination of drugs would be most effective in people, Itzhaki said.

Pass it on: Antiviral drugs that target the herpes virus may reduce damage caused by Alzheimer's disease.

Follow MyHealthNewsDaily staff writer Rachael Rettner on Twitter @RachaelRettner. Find us on Facebook.

Rachael Rettner

Rachael is a Live Science contributor, and was a former channel editor and senior writer for Live Science between 2010 and 2022. She has a master's degree in journalism from New York University's Science, Health and Environmental Reporting Program. She also holds a B.S. in molecular biology and an M.S. in biology from the University of California, San Diego. Her work has appeared in Scienceline, The Washington Post and Scientific American.