The team found more viral DNA in Alzheimer's brains compared with healthy brains-specifically, high levels of DNA from human herpesvirus 6A (HHV-6A).
Researchers in the United States believe the disease may trigger an immune "cascade" which encourages the growth of amyloid plaques.
The findings were based on a large-scale analysis at three different brain banks by researchers from the Icahn School of Medicine at Mount Sinai and Arizona State University-Banner Neurodegenerative Disease Research Center (NDRC). While the findings are not causative, they do suggest an interaction between viral DNA sequences and the molecular, genetic, and clinical characteristics of AD.
"The title of the talk that I usually give is, 'I Went Looking for Drug Targets and All I Found Were These Lousy Viruses.' We didn't set out to find what we found". "We were able to use a range of network biology approaches to tease apart how these viruses may be interacting with human genes we know are relevant to Alzheimer's".
Studies have previously suggested that viruses might be linked with Alzheimer's but the new research suggests a relationship between viruses and the activity of genes associated with the disease. Incorporating data from the Emory Alzheimer's Disease Research Center provided insight into viral impact on proteins.
The researchers confirmed their findings with sequencing samples collected by other brain banks, including the Mayo Clinic in Florida and the Religious Orders Study at Rush University in Chicago, observing a persistent abundance of HHV-6A and HHV-7 among Alzheimer's disease patients in those cohorts, too. This analysis allowed us to identify how the viruses are directly interacting with or coregulating known Alzheimer's genes.
They then tried to determine whether viruses are involved in the progression to Alzheimer's or whether they are, instead, bystanders or somehow consequences of the disease; it might have been the case, for instance, that people with Alzheimer's were more susceptible to viral infections.
There may be some new clues as to what lead to Alzheimer's Disease. "But what's clear is that they're perturbing and participating in networks that directly underlie Alzheimer's pathophysiology".
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"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", Dr. Richard J. Hodes, the National Institute on Aging director, said in a press release by the National Institutes of Health, the parent agency.
The Icahn School of Medicine team and collaborators report their findings today in Neuron, in a paper entitled "Multiscale Analysis of Independent Alzheimer's Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks for Human Herpesvirus". HHV-7 infects more than 80 percent of infants, often causing a rash. They identified specific testable pathways and biological networks.
"Previous studies of viruses and Alzheimer's have always been very correlative".
They found that Alzheimer's biology is likely impacted by a complex group of viral and host genetic factors. And the new study suggests at least two.
Carol Zimmerman from the Eastern Shore's Alzheimer's Association says, "One of the things you'll learn there are ways on how to communicate with somebody who is constantly repeating themselves and how to deal with that".
A new study found those with the neurological disorder had twice the levels of two strains of herpes, HHV-6A and HHV-7, than those without the condition. Antiviral drugs could also be explored as a potential preventive treatment.
Study author Professor Dr Sam Gandy added: "This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer's". We also provide support groups for families who are dealing with the diagnosis or people living with the disease.