Viruses that sneak into the brain might play a role in Alzheimer's.

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 that certain viruses — including two extremely common herpes viruses — affect the behavior of genes involved in Alzheimer's.

The idea that 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 that 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.

The study also fits with mounting evidence that how aggressively the brain's immune system defends itself against viruses or other germs may be riskier than an actual infection.

The team from Mount Sinai came up with some viral suspects — by accident. The study, funded by the National Institutes of Health, wasn't hunting viruses but was looking for new drug targets for Alzheimer's. The researchers were using complex genetic data from hundreds of brains at several brain banks to compare differences between people who'd died with Alzheimer's and the cognitively normal.

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, that infect 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 that causes 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 farther: 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.

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 that herpes seemed to deplete. Sure enough, the animals developed more of those amyloid plaques.