Boston Globe (June 24, 2018): As Drug Development Flounders, People Fearing Alzheimer’s Embrace Lifestyle Changes

It has long been a controversial theory about Alzheimer’s disease, often dismissed by experts as a sketchy cul-de-sac off the beaten path from mainstream research.

But a new study by a team that includes prominent Alzheimer’s scientists who were previously skeptics of this theory may well change that. The research offers compelling evidence for the idea that viruses might be involved in Alzheimer’s, particularly two types of herpes that infect most people as infants and then lie dormant for years.

The study, published Thursday in the journal Neuron, found that viruses interact with genes linked to Alzheimer’s and may play a role in how Alzheimer’s develops and progresses.

The authors emphasized they did not find that these viruses cause Alzheimer’s. But their research, along with another soon-to-be-published study, suggests that 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.

“These viruses are probably significant players in driving the immune system in Alzheimer’s,” said Joel Dudley, the study’s senior author and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mount Sinai in New York. “I think they’re like gas on the flames of some pathology that may be immune-driven.”

If so, that could change the course of research and possibly lead to treatments and new ways of screening for the disease.

“This definitely brings up the potential role of infection or infectious particles in the pathology of Alzheimer’s,” said Dr. John Morris, director of the Knight Alzheimer’s Disease Research Center at Washington University School of Medicine in St. Louis.

Dr. Morris, who was not involved in the research, said it provided the strongest evidence to date for a viral role.

www.nytimes.com/2018/06/21/health/alzheimers-virus-herpes.html?hpw&rref=…

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