Researchers from the Icahn School of Medicine at Mount Sinai have found that herpesviruses are more abundant in the brains of Alzheimer’s patients and suggest that they may play a role in regulatory genetic networks that lead to the disease.
In a large-scale analysis published in Neuron, researchers looked at data from 3 major brain banks provided by National Institutes of Health's Accelerating Medicines Partnership -- Alzheimer's Disease (AMP-AD) consortium. Although initially, they were looking for drugs to repurpose for Alzheimer’s treatment, the data directed them towards investigating viral biology themes.
They analyzed raw genomic data in different groups of patients and constructed, mapped, and compared regulatory gene networks in parts of the brain affected by Alzheimer’s, along with looking at DNA, RNA, and proteins.
The results indicated that human herpesvirus DNA and RNA were more abundant in brains of individuals diagnosed with Alzheimer’s postmortem and the abundance “correlated with clinical dementia scores.” Moreover, the viruses strongly connected with Alzheimer’s, HHV-6A and HHV-7, were not as abundant in individuals with other degenerative brain disorders.
HHV-6A and HHV-7 are common, often asymptomatic viruses. In fact, according to the researchers, in North America, almost 90% of children have one of these viruses circulating in their blood by the time they're a few years old.
By constructing networks modeling the interaction, researchers showed that viral genes were regulating and being regulated by human genes and that genes associated with increased Alzheimer’s risk were impacted. Additionally, the researchers found that herpesviruses were involved in controlling amyloid precursor proteins which are behind the plaques that build up in the brain infected with Alzheimer’s.
"Previous studies of viruses and Alzheimer's have always been very correlative. But we were able to do statistical causal inference testing and more sophisticated analysis, which allowed us to identify how the viruses are directly interacting with or co-regulating or being regulated by Alzheimer's genes,” co-senior author Joel Dudley, PhD, associate professor of genetics and genomic sciences and director of the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai said in a recent statement.
“I don't think we can answer whether herpesviruses are a primary cause of Alzheimer's disease. But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology,” he added.
The results do not provide an answer on to how to detect herpesviruses that could be related to Alzheimer’s disease nor do they provide information pertaining to treatment. However, the results do provide an opportunity to further explore the viruses and their interactions and how they relate to Alzheimer’s.