NEUROLOGY

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New Evidence that Viruses May Play a Role in Alzheimer’s Disease

 

Alzheimer’s disease (AD) 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 AD, and potentially lead to new treatment strategies.

 

National Institute on Aging (NIA) study finds new evidence that viruses may play a role in AD.

 

According to an article published online in the journal Neuron Analysis (21 June 2018), large data sets from post-mortem brain samples of people with and without AD has revealed new evidence that viral species, particularly herpesviruses, may have a role in AD biology. The study harnessed data from brain banks and cohort studies participating in the Accelerating Medicines Partnership – Alzheimer’s Disease (AMP-AD) consortium. The authors emphasized that while their findings do not prove that the viruses cause the onset or progression of AD, the findings do show that viral DNA sequences and activation of biological networks — the interrelated systems of DNA, RNA, proteins and metabolites — may interact with molecular, genetic and clinical aspects of AD.

 

The authors originally set out to find whether drugs used to treat other diseases can be repurposed for treating AD, and designed the study to map and compare biological networks underlying AD. What they found is that AD biology is likely impacted by a complex constellation of viral and host genetic factors, adding that there are specific testable pathways and biological networks. The authors 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 authors made several key findings, including:

Human herpesvirus 6A and 7 were more abundant in Alzheimer’s disease samples than non-Alzheimer’s.

 

There are multiple points of overlap between virus-host interactions and genes associated with Alzheimer’s risk.

 

Multiple viruses impact the biology of Alzheimer’s disease across domains such as DNA, RNA and proteins.

Important roles for microbes and viruses in Alzheimer’s disease have been suggested and studied for decades. Since the 1980s, hundreds of reports have associated AD 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 AD. 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 AD.

 

More on this research is available in announcements from the Icahn School of Medicine at Mount SinaiArizona State University and Cell Press, the publisher of Neuron.

 

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