By Mark Terry


The predominant theory behind the cause of Alzheimer’s is that an accumulation of a protein called beta-amyloid disrupts synapses and causes the cognition problems and brain damage seen in the disease. Late in the disease, another protein, tau, is observed. But there are other theories, including viruses, and a recent study published in the journal Neuron supports that theory.

Researchers from the Icahn School of Medicine at Mount Sinai evaluated data on the brains of 622 people who had indications of Alzheimer’s and 322 people who did not. They found levels of herpes virus in the Alzheimer’s patients that were up to twice as high as the non-disease group.

Joel Dudley, co-author of the study, said in a statement, “I don’t think we can answer whether herpes viruses are a primary cause of Alzheimer’s disease. But what’s clear is that they’re perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer’s topology.”

Dudley told CNN, “The title of the talk that I usually give is, ‘I Went Looking for Drug Targets, and All I Found Were These Lousy Viruses.’”

He suspects the study results could assist in identifying virus biomarkers that might help diagnose Alzheimer’s and assess an individual’s risk for the disease.

“This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer’s,” said co-author Sam Gandy, professor of neurology and psychiatry and director of the Center for Cognitive Health at Mount Sinai in New York, reports CNN.

They point out that this set of herpes viruses is common and that about 90 percent of adults have been exposed to the herpes virus by age 50. Gandy said, “While these findings do potentially open the door for new treatment options to explore in a disease where we’ve had hundreds of failed trials, they don’t change anything that we know about the risk and susceptibility of Alzheimer’s disease or our ability to treat it today.”

The two herpes viruses observed were herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7). Both strains are related and, according to the HHV-6 Foundation, infect almost 100 percent of human beings, typically before the age of three. This often results in fever, diarrhea, and sometimes roseola, a specific rash. The foundation notes that these viruses, like other herpesviruses such as Epstein Barr, chicken pox, and herpes simplex, they establish “life-long latency and can become reactivated later in life.” It can occur in the brain, lungs, heart, kidney and gastrointestinal tract, especially in patients with immune deficiencies and organ transplants. It also points out that HH-6 reactivation “in the brain tissue can cause cognitive dysfunction, permanent disability and death.”

So, the question clearly remains, Is the increase of the virus in the brains of Alzheimer’s patients a precursor to the disease, or a reflection of compromised immune systems? That’s a chicken or egg question. It’s entirely possible there’s a complex interplay of accumulation of beta-amyloid, the immune system, and whatever viruses may be present in the brain. It was only about a week ago that French researchers identified a mechanism behind how amyloid aggregates change the usual function of neuronal connections by interacting with an enzyme involved in synaptic plasticity.

Keith Fargo, director of scientific programs and outreach for the Alzheimer’s Association, notes that much more work would need to be done to prove a connection between herpes viruses and Alzheimer’s. “However, if viruses or other infections are confirmed to have roles in Alzheimer’s, it may enable researchers to find new antiviral or immune therapies to treat or prevent the disease. The Alzheimer’s Association welcomes new ideas in the Alzheimer’s field and new avenues to pursue for potential treatments and prevention strategies.”



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