How do viruses affect Alzheimer's

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American researchers found ‘unusually high‘ levels of two strains of human herpes virus 6A (HHV-6A) and human herpes virus 7 (HHV-7) in brains of Alzheimer’s sufferers, compared to those free of the disease. This opens up a robust array of new targets in the search for a cure to 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 coregulating or being regulated by Alzheimer’s genes. 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,” says Dudley. 

The researchers believe that their findings align with other current research in the Alzheimer’s field on the role of innate immunity in the disease, particularly recent findings that beta-amyloid protein–the culprit behind the plaques that build up in the Alzheimer’s-affected brain–may accumulate as part of a defense against infections. In their study, they found that herpesviruses were involved in networks that regulate amyloid precursor proteins.
No New WorriesThey argue, however, that their work shouldn’t make anyone worried. “While these findings do potentially open the door for new treatment options to explore in a disease where we’ve had hundreds of failed trials, they don’t change anything that we know about the risk and susceptibility of Alzheimer’s disease or our ability to treat it today,” says co-senior author and Alzheimer’s disease specialist Sam Gandy. 

This is especially true because HHV-6A and HHV-7 are extremely common and often latent or asymptomatic: 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. “There are still a lot of unanswered questions around how we go from being able to detect it circulating in someone’s blood to knowing whether it’s active in a state that might be relevant to Alzheimer’s disease,” says Readhead.
Alzheimer’s & Viruses: Specific and TestableBut even if questions remain, this research offers strong support for a long-controversial hypothesis that viruses might be involved in the development of Alzheimer’s disease. “We didn’t have a horse in this virus race whatsoever. It’s the data that took us there. And now, not only is the viral hypothesis resurrected: it has specific testable pathways and networks and interactions that can be explored and reconciled with the rest of the work emerging in Alzheimer’s,” says Dudley. 

“All these Alzheimer’s brains in these separate, major brain banks have previously unsuspected substantial populations of herpesvirus genomes and that deserves an explanation wherever it falls in the pathogenesis. It doesn’t deserve to just be brushed away,” says Gandy.

“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 that lends support to this line of inquiry,” said NIA Director Richard J. Hodes, M.D. “This research reinforces the complexity of Alzheimer’s disease, creates opportunities to explore Alzheimer’s more thoroughly, and highlights the importance of sharing data freely and widely with the research community.” 

Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks. More evidence is accumulating to indicate that this loss of cognitive functioning 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 in Alzheimer’s, and potentially lead to new treatment strategies. 

The research group, which included experts from Icahn School of Medicine at Mount Sinai, New York City, and Arizona State University, Phoenix, originally set out to find whether drugs used to treat other diseases can be repurposed for treating Alzheimer’s. They designed their study to map and compare biological networks underlying Alzheimer’s disease. What they found is that Alzheimer’s biology is likely impacted by a complex constellation of viral and host genetic factors, adding that they identified specific testable pathways and biological networks.
Robust Findings“The robust findings by the Mount Sinai team would not have been possible without the open science data resources created by the AMP-AD program–particularly the availability of raw genomic data,” said NIA Program Officer Suzana Petanceska, Ph.D., who leads the AMP-AD Target Discovery and Preclinical Validation Project. “This is a great example of the power of open science to accelerate discovery and replication research.” 

The researchers used multiple layers of genomic and proteomic data from several NIA-supported brain banks and cohort studies. They began their direct investigation of viral sequences using data from the Mount Sinai Brain Bank and were able to verify their initial observations using datasets from

• The Religious Orders Study
• The Memory and Aging Project and
• The Mayo Clinic Brain Bank.

They were then able to incorporate additional data from the Emory Alzheimer’s Disease Research Center to understand viral impacts on protein abundance. Through the application of sophisticated computational modeling the researchers made several key findings, including:

1. Human herpesvirus 6A and 7 were more abundant in Alzheimer’s disease samples than non-Alzheimer’s.
2. There are multiple points of overlap between virus-host interactions and genes associated with Alzheimer’s risk.
3. Multiple viruses impact the biology of Alzheimer’s disease across domains such as DNA, RNA and proteins.

No Evidence to Reassess RiskImportant roles for microbes and viruses in Alzheimer’s disease have been suggested and studied for decades, the authors noted. Since the 1980s, hundreds of reports have associated Alzheimer’s with bacteria and viruses. These studies combined suggest a viral contribution but have not explained how the connection works. 

While the current findings are more specific, they do not provide evidence to change how risk and susceptibility are assessed, nor the diagnosis and treatment of Alzheimer’s, the authors said. Rather, the research gives scientists reason to revisit the old pathogen hypothesis and will be the basis for further work that will test whether herpes virus activity is one of the causes of Alzheimer’s.

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