ASU researchers are looking at new links between viruses and Alzheimer's

ASU scientists are examining the presence of viruses in the brain and how they might contribute to Alzheimer’s disease

ASU researchers are looking deeper into what might be effecting Alzheimer's disease (AD), an irreversible, chronic neurodegenerative disease that has symptoms including memory loss and dementia.

These researchers are looking at the disease from different directions, focusing on the presence of viruses in the brain and how they might contribute to the disorder. 

Benjamin Readhead is an assistant research professor at the ASU’s Neurodegenerative Disease Research Center (NDRC) and lead author of a multi-scale analysis of independent Alzheimer’s cohorts, recently published in science journal Neuron.

He said that this whole area of study is something called the Alzheimer's Pathogen Hypothesis, which essentially is the idea that pathogens in some form, whether they are viruses, bacteria, fungi, etc., might in some way contribute to either the risk that someone might have for developing AD, or the rate in which it might progress once the disease is established.

Readhead said that the central question of the pathogen hypothesis is whether or not these viruses are actually causing or associated with the disease. 

“We actually began this study with a certain goal for new treatments for people living with Alzheimer's disease,” Readhead said. “Originally this study started off as a drug repurposing study. We were interested in seeing whether or not there might be ways that we could repurpose existing medications that could have been developed for other indications but used in Alzheimer's disease … We started to analyze our results and realize that we're actually getting a lot of clues from a lot of different directions that suggested to us that some kind of viral activity might be explaining what it was we were seeing.”

Diego Mastroeni is an Assistant Research Professor in the School of Life Sciences, focusing on fields of Neuroscience and Alzheimer's. He is currently researching and examining genetic changes within the brain regions affected early in Alzheimer's disease and Parkinson's disease. 

His study is shedding new light on the genetic basis of glial dysfunction in dementia and could lead to more targeted therapies for Alzheimer's and Parkinson's diseases.

He said that the real question is, why is it important that researchers look into new factors that might contribute to Alzheimer’s?

“One hundred years ago Alois Alzheimer discovered the hallmarks of Alzheimer’s disease, plaques and tangles,” Mastroeni said in an email. “Here we are a century later still focusing on the exact same pathological features Alois Alzheimer described on a basic light microscope.”

Mastroeni said that researchers have highly sophisticated equipment available to use and the most imaginative neuroscientists the world has ever seen. 

But despite all these resources, researchers still focus on the things that are the most obvious. 

“The vast majority of therapeutics put into clinical trials for AD have focused on Aβ and, to a lesser extent, tau,” Mastroeni said in an email. “All, to date, have failed. Anti-inflammatory approaches have also been pursued in rigorous clinical studies, with similar results.”

Readhead said that since AD has such a long pre-disease course, looking at the disease from its various states and seeing whether or not these kind of viral signals exist is going to be really important for researchers.

He said that they conducted a multi-scale multi-cohort network analysis. 

This means that they looked at many different data sets and tried to apply a range of different computational approaches to try and uncover important relationships between viruses that they were detecting in these brain samples and all the different levels of post biology.

“We're interested in looking for connections between viruses in genes and proteins at a molecular level,” Readhead said. “We were also interested in looking at viral impacts on high level aspects of the disease, like the severity of tangles and flux in the disease.”

Readhead said they they are also interested in trying to understand relationships between viruses and clinical aspects of the disease.

“What we found actually was really a complex web of interactions between different viruses with other viruses, also with molecules that are molecules and genes and proteins that are just part of normal host biology,” Readhead said. “What we saw is there are actually many common viral species that … (are present) in a normal aging brain.”

Readhead said that a huge breakthrough in their research was finding an increase abundance of two, typical human herpes viruses, herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7). There was an increased abundance of these two viruses in the brains of people that died with Alzheimer's disease compared with normal individuals.

Mastroeni said that recent research, out of his and Dr. Readhead’s labs, has implicated a potential viral link to the pathogenesis of Alzheimer’s disease. 

“Although significant work needs to be done before one can be confident in the viral story, this is a fresh idea that demands further investigation,” Mastroeni said in an email.

Readhead said that, at this stage, the findings from his research is more of a scientific contribution rather than a medical contribution.

"What we found does not change what we know about risk factors for Alzheimer's, nor how we would go about diagnosing or treating it at this stage," Readhead said. "There's a lot of careful science we need to do to go from being able to know what it means to have been infected, to know what the implications of that are in terms of why it is that some of these viruses end up in a higher abundance in some people's brains than others."

He said that what researchers are reporting isn't something that is going to change clinical treatment in the near future.

"What these findings do give us (are) some very testable hypotheses that we think deserve to be carefully considered and studied further to really understand how plausible the pathogen hypothesis for Alzheimer's might be."


Reach the reporter at jlmyer10@asu.edu or follow @jessiemy94 on Twitter. 

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