top of page
Leaf Pattern Design

Do Viruses Lead to Alzheimer's?

Updated: Jan 11, 2019



Do Viruses Lead to Alzheimer's?

Herpesviruses: A group of viruses that contain DNA and cause infections. Well, what is the connection between herpesviruses and dementia? Researchers at the Icahn School of Medicine at Mount Sinai in New York City, NY, and Arizona State University in Phoenix - found that the brains of people with Alzheimer’s had more herpesviruses (HHV-6A and HHV-7) compared to people who didn’t have Alzheimer’s. In this groundbreaking study, researchers explore one of the culprits of Alzheimer’s: viruses.


A paper on this research was published on June 21, 2018 in the scientific online journal Neuron. In this paper, the researchers state that they have utilized large amounts of data from brain donors to analyze the genes that are inherited and those that are turned on or off in a person who has developed Alzheimer’s. What they found was that certain species of herpesviruses (HHV-6A and HHV-7)contribute to the development of Alzheimer’s. The National Institute of Health (NIH) sponsored Accelerated Medicines Partnership for Alzheimer's Disease (AMP-AD) funded the research and also contribute DNA and RNA sequencing data to the experiment. They provided data from 622 brain donors who had Alzheimer's and 322 brain donors who didn’t have the disorder. According to Arizona State University, “ The whole DNA sequencing was used to provide detailed information about each person’s inherited genes. RNA sequencing from several brain regions was used to provide detailed information about the genes that are expressed differently in donors with and without the disease. The study identifies high levels of human herpesvirus (HHV) and in brain samples showing signs of Alzheimer, compared to the lower levels found in normal brains”. The data that the researchers have gathered have been replicated in many samples including at Mayo Clinic Brain Bank, Banner-Sun Health Research Institute's Brain and Body Donation Program, and the Rush Alzheimer’s Disease Center.


The exploration of viruses are currently a popular topic in neuroscience. However, more research and evidence needs to be gathered to determine whether they have a direct cause on developing Alzheimer’s or they just manifest in the human brain due to neural deterioration. Joel Dudley, associate professor of Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai, associate research professor in the Neurodegenerative Disease Research Center (NDRC) states that, “ 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 and participating in networks that directly underlie Alzheimer’s pathophysiology”. Amyloid ( a protein) causes plaque to build up in the brain, and tau (a protein) causes neurofibrillary tangles to form. These two characteristics are what is used to diagnose Alzheimer’s. Relating this to the study,  Ben Redhead, assistant research professor in the NDRC, housed at Arizona State University’s Biodesign Institute explains, “ a number of viruses looked interesting. We saw a key virus HHV 6A, regulating the expression of quite a few Alzheimer’s (AD) risk genes and genes known to regulate the processing of amyloid, a key ingredient in AD neuropathology”.


This research is pointing us in the right direction for Alzheimer’s research. The key findings of this study include, HHV-6A and HHV-7 were the most abundant in Alzheimer’s brain donors than brain donors who didn’t have the disorder,  there were multiple places where the “virus-host interactions and genes associated with Alzheimer’s” overlapped, and multiple viruses impacted the biology of Alzheimer's. The National Institute on Aging Director Richard J. Hodes, M.D. reiterates, “ This research reinforces the complexity of Alzheimer’s, created the opportunity to explore Alzheimer’s more thoroughly, and highlights the importance of sharing data freely and widely with the research community”.

 

References:

Comments


Commenting has been turned off.
bottom of page