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. Since the 1980s, hundreds of reports have associated Alzheimer's with bacteria and viruses.
Alzheimer's disease has been linked with the presence of high levels of herpes viruses in the brain.
Keith Fargo, the Alzheimer's Association's director of scientific programs and outreach, said that more research will need to be done to prove that there is a connection between herpes viruses and Alzheimer's.
"This study illustrates the promise of leveraging human brain samples, emerging big data analysis methods, converging findings from experimental models, and intensely collaborative approaches in the scientific understanding of Alzheimer's disease and the discovery of new treatments", said study co-author Eric Reiman, executive director of the Banner Alzheimer's Institute and university professor of neuroscience at ASU.
Experts stressed it was not clear if the viruses caused dementia or were caused by it.
The quest to understand what causes Alzheimer's disease-and to treat it-is complicated by the disease's long, slow progression and the difficulty of collecting brain tissue samples.
This undated photo provided by Mount Sinai Health System shows slices of human brains in the Mount Sinai Brain Bank that researchers are using to study Alzheimer's disease. The constructed virus-host protein networks also suggested that herpesvirus interaction perturbed cell nucleotide pools, tRNA synthesis, and protein translation, "which suggested a picture of virally induced dysregulation of nucleotide pool metabolism, especially purine bases, consistent with several metabolomics studies in AD". Once combined, the data revealed a "consistently increased abundance of HHV-6A and HHV-7, driven mainly by the "unique" region of each virus", the researchers wrote. Alzheimer's is the sole disease in the top 10 United States causes of death that has no significant treatment available. In March 2016 in the Journal of Alzheimer's Disease, 33 global scientists penned an editorial urging the research community to seriously consider the idea that pathogens could be involved. "Collectively, these findings support the role of miR-155 as a key node in host response to AD-relevant viral perturbation, and as a potential mediator of neuronal loss", they state. "What I believe is that in genetically or physiological susceptible individuals, the virus is acting as an agonist of the disease", Dudley says-a number of processes likely participate, with viruses being just one piece of the puzzle.
Yet even if viruses only abet disease progress, that realization could open the door to better ways to diagnose and treat Alzheimer's. "This is is also consistent with the contribution of viral perturbation in driving the preclinical AD transcriptional phenotype, given that our prioritization of miR-155 was informed by findings in the preclinical AD networks". With Harvard colleague Dr. Robert Moir, Tanzi has performed experiments showing that sticky beta-amyloid captures invading germs by engulfing them - and that's why the plaque starts forming in the first place.
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.
Dudley and his colleagues stumbled across this possible viral link to Alzheimer's during an analysis meant to find ways that drugs used to treat other illnesses could be repurposed for treating the dreaded neurodegenerative disease.
But Dudley is willing to accept the risks and push forward.
"The title of the talk that I usually give is, 'I Went Looking for Drug Targets and All I Found Were These Lousy Viruses, '" explains Joel Dudley, co-senior author on the study. "But the data are the data".