Do Viruses Play a Role in Alzheimer's?
The brain tissue holds the clues. Analysis of large data sets from post-mortem brain samples of people with and without Alzheimer’s disease revealed new evidence that viruses, particularly herpesviruses, may play a role.
Researchers funded by the National Institute on Aging made the discovery from brain banks and cohort studies made available via the Accelerating Medicine Partnership for Alzheimer’s Disease. The partnership involves six academic medical centers, including an Emory team led by Holland Professor of Neurology Allan Levey, director of the Goizueta Alzheimer’s Disease Research Center, and Nick Seyfried, Emory assistant professor of biochemistry and neurology. The study included data from the Goizueta center.
The authors emphasize that their findings, reported in the June 21 issue of Neuron, do not prove that viruses cause the onset or progression of Alzheimer’s, but rather, that they interact in ways not yet fully understood. “The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence based on unbiased approaches and large data sets,” says NIA Director Richard Hodes. “This reinforces the complexity of Alzheimer’s disease.”
Evidence is accumulating that the loss of cognitive functioning during Alzheimer’s is a mix of many different disease processes in the brain rather than just one, such as buildup of amyloid or tau proteins.
Identifying links to viruses may help researchers learn more about the complicated biological interactions involved and lead to treatment strategies. Through computational modeling the researchers made several findings, including:
■ Human herpesviruses 6A and 7 were more abundant in Alzheimer’s disease samples than in non-Alzheimer’s.
■ Multiple points of overlap exist between virus-host interactions and genes associated with Alzheimer’s risk.
■ Multiple viruses impact the biology of Alzheimer’s disease across domains.
