The research was carried out at Waterford Institute of Technology
23 June, 2018, 02:48
Using computational tools to analyze these large datasets, the researchers were able to generate a picture of the genetic, transcriptional, and molecular networks that underpin AD development and progression and how viruses are potentially involved. One of the primary questions is whether such pathogens play an active, causative role in the disease or enter the brain simply as opportunistic passengers, taking advantage of the neural deterioration characteristic of AD.
Researchers at the Icahn School of Medicine in NY and Arizona State University in Tempe conducted RNA sequencing on data from 3 brain banks to evaluate differential viral abundance in AD.
"We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain", Dudley says.
"We didn't go looking for viruses, but viruses sort of screamed out at us", said lead author Ben Readhead, of Arizona State University.
"We needed access to sequences that are usually discarded in the course of studying the human genome".
The study, headed by a team at the Icahn School of Medicine at Mount Sinai, found increased levels of the two Roseoloviruses, human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV7), interacting with gene networks in areas of the brain that are known to be affected in AD. "We saw a key virus, HHV-6A, regulating the expression of quite a few AD risk genes and genes known to regulate the processing of amyloid, a key ingredient in AD neuropathology".
The study homed in on two specific herpes viral strains that were most specifically abundant in the brains of Alzheimer's sufferers, HHV-6A and HHV-7.
While this study does not demonstrate that viruses are linked causally to Alzheimer's disease, it may be the most compelling evidence pointing to a viral contribution ever presented, Gandy noted. The study points to the viruses as possible accomplices that drive disease progression but does not suggest that Alzheimer's may begin after they are transmitted through casual contact. "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", said study coauthor Joel Dudley, PhD, in a statement.
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.
The study found that herpes viruses were involved in networks that regulate amyloid precursor proteins.
They argue, however, that their work shouldn't make anyone anxious.
This is especially true because HHV-6A and HHV-7 are extremely common and often latent or asymptomatic.
A new study links certain viruses, called HHV-6 and HHV-7, with Alzheimer's disease. "We didn't have a horse in this virus race whatsoever. But it would be negligent for us to ignore these results until the next study reports back, which will take several years".
It is estimated that by 2050, almost 14 million Americans will be living with Alzheimer's disease. Dudley has met researchers at conferences who have confided in him that they have also collected data implicating pathogens in the disease but that they have been too scared to publish-for fear that they will be ostracized by the Alzheimer's community.
The new research is the fruitful result of close working relationships among researchers from Arizona State University, Banner, Mount Sinai and other research organizations, as well as public-private partnerships in AMP-AD.
Dr David Reynolds, chief scientific officer at Alzheimer's Research UK, said the viruses highlighted in the study were not the same as those that caused cold sores.
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