That’s according to new research published Thursday in the journal Neuron, for which a team of scientists at the Icahn School of Medicine at Mount Sinai, New York, used genetic data from three different brain banks to examine differences between healthy brain tissue and brain tissue from individuals who died with Alzheimer’s.
The medical community still doesn’t know what causes the disease, so the Mount Sinai scientists set out to try and identify new targets for drugs. Instead, they stumbled upon repetitive hints that the brain tissue of Alzheimer’s patients had higher levels of viruses.
“The title of the talk that I usually give is, 'I Went Looking for Drug Targets and All I Found Were These Lousy Viruses,’” study co-author and geneticist Joel Dudley said in a statement.
While studying brain tissue of 622 people who had signs of the disease and 322 who weren’t affected by it, Dudley and his team found significant evidence suggesting two specific strains of the human herpes virus (HHV-6A and HHV-7), both of which commonly cause skin rashes called roseola in young children, may have seeped into the Alzheimer’s patients’ brains and remained inactive for decades.
“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 said.
The team found that the herpes virus genes were interacting with specific genes known to increase risk for Alzheimer’s, but the mere presence of the virus isn’t enough to lead to the disease. Instead, Dudley said, something needs to be activating the viruses to cause replication.
But their findings do align with some other current research, specifically regarding beta-amyloid proteins, proteins known to increase plaque buildup in Alzheimer’s-affected brains. In the new study, the researchers noted that herpes viruses were involved in networks that regulate these amyloid precursor proteins.
The National Institute on Aging, which helped fund the new research, is working to back another study to test the effects of antiviral drugs on people in the early stages of Alzheimer’s with high levels of herpes virus in their brains.
While the study findings open a door for new treatment options, co-senior author Sam Gandy said in a statement, the results don’t exactly change what scientists know about the risk and susceptibility of Alzheimer’s or their ability to treat it. That’s because both HHV-6A and HHV-7 are incredibly common. In North America alone, almost 90 percent of children have one of the viruses in their blood by the time they’re a few years old, according to Gandy.
According to 2017 report from the Atlanta-based Centers for Disease Control and Prevention, the death rate from Alzheimer’s disease has risen by 55 percent in recent decades.
Patients, caregivers and publicly funded long-term care facilities bear significant financial and societal costs due to the increasing rates of Alzheimer’s deaths.
Experts recommend more federal funding for caregiver support and education and for research to find a cure.
According to the CDC, it’s estimated the U.S. spent some $259 billion in 2017 on costs related to the care of those with Alzheimer’s and other forms of dementia.