Discovery about virus, Alzheimer’s could open new treatment avenues
Researchers may have found a tiny culprit— human herpes virus—in the progressive loss of memory, thinking ability and identity that comes with Alzheimer’s disease. And it could be a big deal.
In research that revives a suspicion first raised more than six decades ago, scientists have found higher levels of the common virus in the brains of people who had both behavioral symptoms and neurological evidence of Alzheimer’s at the time of their death than in the brains of deceased donors who had no signs of dementia.
The researchers’ suspicions fell upon two strains of herpes virus—herpesvirus 6A and herpesvirus 7—that were most evident in regions of the brain affected first in Alzheimer’s disease, and in those that suffer most as the disease progresses.
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. It was published in the journal Neuron.
An estimated 5.7 million Americans are living with Alzheimer’s disease in 2018, a number expected to rise to 14 million by 2050 unless some means of prevention or treatment is found.
The findings are a far cry from establishing what role the two strains of the virus might play in initiating or driving the decades-long process of cognitive loss and brain changes in Alzheimer’s, or even if they play such a causative role. But it gives researchers a new foothold in a field of research that has failed to find anything to prevent, slow or reverse Alzheimer’s inexorable march.
“It is a beautiful piece of work, but it is still an association,” said Miroslaw Mackiewicz, program director at the National Institute on Aging’s Division of Neuroscience. Still, added Mackiewicz, by providing evidence for the virus’ presence and some hints at its possible role, “you have some way to start your experiments.”
If further research uncovers a key role of herpes virus in Alzheimer’s disease, “this would generate a lot of excitement because we have vaccines” against various strains of disease-causing herpes virus, said Mackiewicz.