- The Washington Times - Thursday, June 21, 2018

Alzheimer’s researchers have discovered a link between the herpes virus and the degenerative neurological disease, a breakthrough that offers the hope of an eventual cure.

The scientific discovery could open a door a new treatment strategy to attack the most common form of dementia that affects more than 5 million people in the U.S.

“This work resurrects and points out an older concept that was not proven: that viruses cause Alzheimer’s disease,” said Miroslaw Mackiewicz, a program director of the Division of Neuroscience at the National Institute on Aging, part of the National Institutes of Health.

Alzheimer’s is a progressive disease. Dementia symptoms gradually worsen from mild memory loss to the potential loss of the ability to carry on a conversation and respond to the surrounding environment, according to the Alzheimer’s Association.

Researchers from the Icahn School of Medicine at Mount Sinai, New York, and Arizona State University in Phoenix originally meant to test whether available drugs for other diseases could work in treating Alzheimer’s.

Instead, they discovered an overabundance of two viruses: human herpesvirus (HHV) 6a and 7. These viruses are believed to be common in the population, with nearly all children contracting them. Symptoms usually are manifested as a fever and rash.

Not everyone will get sick, and the virus can lie dormant. However, it is also known to cause neurological disorders such as febrile seizures, encephalitis or intractable seizures, according to the HHV-6 Foundation.

“These viruses can affect neurons, and they’re actually quite efficient at it,” said Joel Dudley, one of the co-authors of the study and director of the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai.

The study, published in the journal Neuron on Thursday, doesn’t state that the viruses cause Alzheimer’s but that strong evidence shows it plays an important role among the complex interactions of disease progression.

“I think it’s clearly participating in the pathology, but it’s not clear that it’s a primary cause,” Mr. Dudley said. “In fact, there could be a little spark of disease and that these viruses act like gasoline on the spark in a genetically susceptible individual.”

This understanding, of illuminating the building blocks of Alzheimer’s, is a key part of efforts of the Accelerating Medicines Partnership, an initiative that brings together the NIA and NIH with industry and nonprofit foundations to provide unprecedented resources for information-sharing and increase funding for research and clinical trials.

The Centers for Disease Control and Prevention estimates that about 5 million people in the U.S. were living with Alzheimer’s in 2013. That number is expected to balloon to 14 million by 2050.

Over the past few decades, researchers and doctors have made major advancements in early detection and diagnosis of the disease, with high-resolution brain imaging, spinal taps and even smell tests able to detect preclinical Alzheimer’s, said Dr. D.P. Devanand, professor and director of Geriatric Psychiatry at Columbia University Medical Center.

Treatment, however, remains woefully inadequate.

“In terms of treatment, we haven’t really made that much progress, and the viral hypothesis of Alzheimer’s disease has only recently begun to be investigated,” he said.

Conventional Alzheimer’s treatments focus on finding a way to disrupt and reduce the buildup of two proteins — beta-amyloid and p-tau — that clog neural pathways and are responsible for symptoms that typically start as careless forgetfulness but deteriorate to devastating memory loss and emotional and physical instability.

The problem is, while some of these medications do decrease protein buildup in the brain, the patient rarely shows improvement in physical and mental symptoms. Options such as medications to treat symptoms of depression, anxiety and hallucinations act as a temporary Band-Aid. Others, such as anti-psychotic medications, carry a high fatality risk.

While not involved in the latest research, Dr. Devanand applauds the scientists for bringing more awareness and legitimacy to an idea that has long been on the fringes of Alzheimer’s research.

“Now with expanded funding, what can happen is more risky and seemingly far-fetched ideas can be funded to see whether something out of the mainstream works or not,” he said.

The NIA has provided funding for Dr. Devanand’s own study. Years earlier, he said, it would have been difficult to get support. His phase two clinical trial, currently enrolling patients, will test to see if Valtrex, the anti-viral medication for oral and genetical herpes, can have an affect on Alzheimer’s patients.

“When funds were more limited, an anti-viral drug trial would have been harder to get funded, he said. “I tried one or two things in the past some years ago, and it was hard to get funded because reviewers were skeptical.”

Leaders at the NIA said the latest research supports the mission started nearly seven years ago.

“The robust findings by the Mount Sinai team would not have been possible without the open science data resources created by the [Accelerated Medicine Project-Alzheimer’s Disease] program — particularly the availability of raw genomic data,” NIA program officer Suzana Petanceska, who leads the AMP-AD Target Discovery and Preclinical Validation Project, said in a statement.

“This is a great example of the power of open science to accelerate discovery and replication research.”

Mr. Dudley said his team’s findings give more weight to other studies that have suggested a link between the immune system and Alzheimer’s, but where associations were viewed as weak.

“It further strengthens the idea that immune system plays a role in Alzheimer’s, which is pretty important because it’s a big paradigm shift from the sort of, purely neurological view of Alzheimer’s,” he said.

“I think this theory that has been sitting on the fringes of Alzheimer’s for probably 20 years at this point is finally mainstream — has finally crossed over. That’s important. There will be a lot more research.”

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