Virus Infections in Early Life Could Set the Stage For Alzheimer’s


Virus Infections in Early Life Could Set the Stage For Alzheimer’s

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.

A new study suggests that certain viruses could kick-start an immune response that might increase the accumulation of amyloid, a protein in human brains which clumps into the telltale plaques of Alzheimer's. The researchers found higher levels of HHV-6A and HHV-7 in Alzheimer's patient brain samples compared with brains unaffected by Alzheimer's.

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. They tested the brain samples from the Mount Sinai Brain Bank, he said and were so surprised at the finding that they tested additional samples from other brain banks and found same results.

Researchers of a new study find evidence that backs the decades-old theory, opening the door for future researches. And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's. Instead they were hoping to pinpoint genes that were unusually active in the brains of people with the earliest stage of Alzheimer's. By mid-century, a new diagnosis will occur every 33 seconds, and costs are expected to exceed $1 trillion annually.

"All these Alzheimer's brains in these separate, major brain banks have previously unsuspected substantial populations of herpesvirus genomes and that deserves an explanation wherever it falls in the pathogenesis", Gandy said. The combined funding support for this five-year endeavor is $185.2 million.

"The viral genomes were detectable in about 30% of Alzheimer's brains and virtually undetectable in the control group", said Sam Gandy, professor of neurology at the Icahn School of Medicine at Mount Sinai, New York and a co-author of the study.

"I look at this paper and it makes me sit up and say, 'Wow, '" said Alzheimer's Association scientific programs director Keith Fargo. "If it becomes evident that specific viral species directly contribute to an individual's risk of developing Alzheimer's or their rate of progression once diagnosed, then this would offer a new conceptual framework for understanding the emergence and evolution of Alzheimer's at individual, as well as population, levels".

"The new study is impressive and very well designed".

The findings don't prove viruses cause Alzheimer's, nor do they suggest it's contagious. "This research reinforces the complexity of Alzheimer's disease, creates opportunities to explore Alzheimer's more thoroughly, and highlights the importance of sharing data freely and widely with the research community". The research team assessed up to 1000 postmortem brains of people who had Alzheimer's disease and those who did not.