New evidence shows viruses may play a role in Alzheimer’s

  • This undated photo provided by Mount Sinai Health System shows slices of human brains in the Mount Sinai Brain Bank that researchers are using to study Alzheimer’s disease. Mount Sinai Health System via AP

Associated Press
Published: 6/21/2018 9:16:01 PM

WASHINGTON — Viruses that sneak into the brain just might play a role in Alzheimer’s, scientists reported Thursday in a provocative study that promises 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 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, said Alzheimer’s specialist Dr. Rudolph Tanzi of Massachusetts General Hospital. With Harvard colleague Dr. Robert Moir, Tanzi has performed experiments showing that sticky beta-amyloid captures invading germs by engulfing them — and that’s why the plaque starts forming in the first place.

The team from Mount Sinai and Arizona State University 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 first clues that viruses were around “came screaming out at us,” said Mount Sinai geneticist Joel Dudley, a senior author of the research published Thursday in the journal Neuron.

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.

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.

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


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