Amid Years Of Dashed Hopes Over Alzheimer’s Breakthroughs, Study Linking Common Virus To Disease Fans Hope
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. Scientists are being very cautious to warn that this might not prove anything, but it's one of the few developments the field has seen in decades.
The New York Times:
A Common Virus May Play Role In Alzheimer’s Disease, Study Finds
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. (Belluck, 6/21)
The Associated Press:
New Evidence That Viruses May 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. (6/21)
Los Angeles Times:
Surprising Discovery About Viruses And Alzheimer’s Disease Could Open New Avenues For Treatment
Their surprise discovery emerged as researchers sorted through a vast genomic data bank in search of new ideas for treating Alzheimer’s with drugs designed for other diseases. The study’s authors pored over DNA and RNA sequencing data from 622 brains donated by people affected by Alzheimer’s and 322 brains that were free of the disease. The data they mined is usually discarded, but was archived instead by the National Institutes of Health in a bid to accelerate the discovery of new treatments by fostering “big data” collaborations. This one brought together scientists at Arizona State University’s Banner Neurodegenerative Disease Research Center and Alzheimer’s experts at New York’s Icahn School of Medicine at Mount Sinai. (Healy, 6/21)
NPR:
Herpes Viruses And Alzheimer's: A Possible Link
Once the researchers knew the viruses were associated with Alzheimer's they started trying to figure out how a virus could affect the course of a brain disease. That meant identifying interactions between the virus genes and other genes in brain cells. "We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain," Dudley says. In essence, he says, they wanted to know: "If the viruses are tweeting, who's tweeting back?" And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's. They also found that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses. (Hamilton, 6/21)
Stat:
Herpes Viruses Could Play Role In Alzheimer's, New Study Finds
During the 14 months that the two studies have been stuck in publication limbo, experimental Alzheimer’s drugs based on the quarter-century-old “amyloid cascade hypothesis” have been flaming out, each more spectacularly than before. (The hypothesis says that production of an aberrant protein called amyloid-beta creates sticky plaques that destroy brain synapses and neurons.) This year alone has brought the demise of the Eli Lilly/AstraZeneca drug lanabecestat; Lilly’s solanezumab; and Merck’s verubecestat. That brings the number of effective Alzheimer’s treatments based on the amyloid cascade hypothesis to … zero, making the need for new ideas more urgent than ever. (Begley, 6/21)
