New evidence some viruses may play a role in Alzheimer's

WASHINGTON -- Viruses sneaking into the brain just might play a role in Alzheimer's, scientists reported Thursday in a provocative study promising to re-ignite some long-debated theories about what triggers the mind-robbing disease.

The findings don't prove viruses cause Alzheimer's, nor do they suggest it's contagious.

But a team led by researchers at New York's Mount Sinai Health System found certain viruses, including two extremely common herpes viruses, affect the behavior of genes involved in Alzheimer's.

The idea infections earlier in life might somehow set the stage for Alzheimer's decades later has simmered at the edge of mainstream medicine for years. It's been overshadowed by the prevailing theory Alzheimer's stems from sticky plaques that clog the brain.

Thursday's study has even some specialists who never embraced the infection connection saying it's time for a closer look, especially as attempts to block those so-called beta-amyloid plaques have failed.

"With an illness this terrible, we cannot afford to dismiss all scientific possibilities," said Dr. John Morris, who directs the Alzheimer's research center at Washington University School of Medicine in St. Louis. He wasn't involved in the new research but called it impressive.

The team found viral genetic material at far higher levels in Alzheimer's-affected brains than in normal ones. Most abundant were two human herpes viruses, known as HHV6a and HHV7, infecting most people during childhood, often with no symptoms, and then lie dormant in the body.

That wasn't unusual. Since 1980, other researchers have linked a variety of bacteria and viruses, including another type of herpes causing cold sores, to an increased risk of Alzheimer's. But it was never clear if germs were merely bystanders or actively spurring Alzheimer's.

The new study went further: Researchers used computer models to check how the viral genes interacted with human genes, proteins and amyloid buildup, almost like the viruses' social media connections, Dudley explained.

"We're able to see if viral genes are friending some of the host genes and if they tweet, who tweets back," Dudley said.

They found a lot of interactions, suggesting the viruses could even switch on and off Alzheimer's-related genes. To see if those interactions mattered, the researchers bred mice lacking one molecule herpes seemed to deplete. Sure enough, the animals developed more of those amyloid plaques.

"I look at this paper and it makes me sit up and say, 'Wow,"' said Alzheimer's Association scientific programs director Keith Fargo.

He said the research makes a viral connection much more plausible but cautioned the study won't affect how today's patients are treated.

If the findings pan out, they could change how scientists look for new ways to treat or prevent Alzheimer's, said Dr. Miroslaw Mackiewicz of NIH's National Institute on Aging. Already, NIH is funding a first-step study to see if an antiviral drug benefits people who have both mild Alzheimer's and different herpes viruses.