Researchers made the discovery after examining data from brain banks and cohort studies that are part of the Accelerating Medicines Partnership — Alzheimer's disease consortium, UPI reported.

But the researchers, who published their findings in the journal Neuron, emphasize that their research doesn't prove that the viruses cause the onset or progression of Alzheimer's.

Currently, no effective prevention or treatment exists for this progressive deterioration of brain tissue, memory and identity, but researchers are hopeful that new, better treatments can emerge as a result of their work.

Dr. Richard J. Hodes, the National Institute on Aging director, said, "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.

"This research reinforces the complexity of Alzheimer's disease, creates opportunities to explore Alzheimer's more thoroughly, and highlights the importance of sharing data freely and widely with the research community."

The loss of cognitive functioning in Alzheimer's disease, an irreversible and progressive brain disorder, has been found to be a mix of different disease processes in the brain, rather than just one, such as buildup of amyloid or tau proteins.

Researchers have been attempting to identify links to viruses and, ultimately, new treatment strategies.

Scientists from Mount Sinai's Icahn School of Medicine and Arizona State University's Banner Neurodegenerative Disease Research Center are seeking to find whether drugs used to treat other diseases can be used for treating Alzheimer's.

Study coauthor Dr. Eric Reiman, executive director of ASU's Banner Alzheimer's Institute, said, "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.”

The team studied DNA and RNA sequencing from 622 brain donors with the clinical and neuropathological features of Alzheimer's disease, and 322 brain donors without the disease.

They found that Alzheimer's biology is likely impacted by a complex group of viral and host genetic factors. They identified specific testable pathways and biological networks.

Dr. Sam Gandy, a professor of neurology and psychiatry at Mount Sinai, said, "This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer's.

"A similar situation arose recently in certain forms of Lou Gehrig's disease. In those patients, viral proteins were discovered in the spinal fluid of some Lou Gehrig's patients, and patients with positive viral protein tests in their spinal fluid showed benefit when treated with antiviral drugs."

Researchers explored viral presence in six key brain regions known to be highly vulnerable to Alzheimer's.

They found that human herpesvirus 6A and seven were up to twice as abundant in Alzheimer's disease samples than non-Alzheimer's ones.

They also found that multiple points overlapped between virus-host interactions and genes associated with Alzheimer's risk, and multiple viruses that impact Alzheimer's disease were found in DNA, RNA and proteins.

Dr. Ben Readhead, an assistant research professor in the NDRC at Arizona State, said, "We didn't go looking for viruses, but viruses sort of screamed out at us.

"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."

Researchers said that previous studies suggest a viral contribution but don't explain how the connection works. They said their findings were more specific but they still don't determine the risk and susceptibility.

Instead, scientists say further work will test whether herpes virus activity is one of the causes of Alzheimer's.

Dr. Joel Dudley, director of the Institute for Next Generation Healthcare at the Icahn School, said, "What this does is further strengthens the emerging theme that DNA immune system plays a role in Alzheimer's and why that gives us hope is that it will reveal a whole set of new potential drug targets for Alzheimer’s and perhaps borrow a lot of the tools and drugs from immunology for Alzheimer's disease.”