Herpes virus may play role in Alzheimer’s, study says

Herpes virus may play role in Alzheimer’s, study says

It's been overshadowed by the prevailing theory that Alzheimer's stems from sticky plaques that clog the brain.

Brains riddled with Alzheimer's disease contain high levels of two strains of human herpes virus, researchers discovered.

Researchers in the U.S. believe the disease may trigger an immune "cascade" which encourages the growth of amyloid plaques. It also suggests that it may be possible to prevent or slow Alzheimer's using antiviral drugs, or drugs that modulate how immune cells in the brain respond to an infection.

"That won't be useful yet", said Alzheimer's disease specialist Dr. Sam Gandy of Mount Sinai Hospital, who helped lead the study team.

They began by sequencing DNA from the dead patients to find out information about inherited genes, followed by finding out how those genes were expressed.

"We didn't go looking for viruses, but viruses sort of screamed at us", states lead author Ben Redhead, assistant research professor at the NDRC.

"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", National Institute on Aging director Richard J. Hodes, MD, said in a statement.

They found that human herpesvirus DNA and RNA were more abundant in the brains of those diagnosed postmortem with Alzheimer's disease and that abundance correlated with clinical dementia scores.

The data provide compelling evidence that these specific viral species contribute to the development of neuropathology and Alzheimer's disease.

The researchers say they found increases in 2 types of herpes viruses in Alzheimer's-affected brains.

"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.

Streetman says there are 34,000 people age 65 or older living with Alzheimer's in the state - and roughly 82,000 people providing uncompensated care.

For the new study, which was broadly created to map and compare genetic, transcriptional, and protein networks underlying AD, the team analyzed whole exome DNA and RNA sequencing data from 622 brain donors with early- and later-stage clinical and neuropathological features of AD, and another 322 brains from donors without the disease, generated through the National Institutes of Health (NIH)-sponsored Accelerated Medicines Partnership for Alzheimer's Disease (AMP-AD).

The research team had been mapping and comparing the biological networks that underlie Alzheimer's disease, based on detailed genetic analyses of more than 600 brain tissue samples. "It could be that things are not as binary as we thought, that viruses act one way and genes another". What they found is that Alzheimer's biology is likely impacted by a complex constellation of viral and host genetic factors, adding that they identified specific testable pathways and biological networks. It seems feasible that amyloid is not the cause of disease in many cases.

"To be clear, it does not prove the idea that viruses causes Alzheimer's".

Researchers said previous studies suggest a viral contribution but don't explain how the connection works.

Gandy and Dudley stress that they don't believe Alzheimer's is an infectious disease that can be transmitted like the common cold.

Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks.

HSV-1 is a different virus from HHV-6A and HHV-7, but Dudley's team did also find that Alzheimer's brains had higher than normal levels of genetic material associated with HSV-1. Ruth Itzhaki, a neurobiologist at the University of Manchester in the United Kingdom, who has led numerous studies linking HSV-1 with Alzheimer's, says she has suffered "derision and vituperative hostility" for pursuing this line of inquiry.

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