In a study, the virus was found to be more prominent in the brains of people who've died with Alzheimer's Disease. The research, published June 21 in Neuron, found convincing signs that certain types of herpes virus may promote the complex process that leads to the disease that afflicts some 5.7 million Americans. 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. "Alzheimer's disease is the largest public health crisis we face and drug companies have so far fallen at every hurdle in finding a solution", he said.
Joel Dudley, a geneticist and genomic scientist at the Icahn School of Medicine at Mount Sinai and senior author of the new paper, had not meant to investigate this theory when his lab began working on the newly published study in 2013.
The nature and significance of viruses and other pathogens in the brain are now hot topics in neuroscience, though the exploration is still in its early stages.
HAMILTON: Joel Dudley is an associate professor at the Icahn School of Medicine at Mount Sinai in NY. "But we were able to perform a more sophisticated computational analysis using multiple levels of genomic information measured directly from affected brain tissue".
"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", Readhead said. Alzheimer's is the sole disease in the top 10 U.S. causes of death that has no significant treatment available. "But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology".
He said the research makes a viral connection much more plausible but cautioned that the study won't affect how today's patients are treated.
"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.
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.
The viruses can cause encephalitis and other chronic conditions.
Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's.
"Sadly, people with dementia and their carers will grasp at any straw and I would worry about the impact of media reports around what seem either naive or deeply cynical attempts to exploit this".
This is especially true because HHV-6A and HHV-7 are extremely common and often latent or asymptomatic.
In the U.S. nine in ten children have one of these viruses circulating in their blood by the time they're a few years old.
But even if questions remain, this research offers strong support for a long-controversial hypothesis that viruses might be involved in the development of Alzheimer's disease.
Prof Dudley said: "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".
Prof Dudley noted the study could potentially translate to the identification of virus, or virus-related, biomarkers that could improve patient risk stratification and diagnosis, as well as implying novel viral targets and biological pathways that could be addressed with new preventative and therapeutic drugs.
Additional contributors to the study include: Center for NFL Neurological Care, Department of Neurology, New York; James J. Peters VA Medical Center, New York; Arizona Alzheimer's Consortium, Phoenix; Department of Psychiatry, University of Arizona, Tucson, AZ; Banner Alzheimer's Institute, Phoenix; Neurogenomics Division, Translational Genomics Research Institute, Phoenix; Institute for Systems Biology, Seattle.
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