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It starts with forgetting things you just learned, but over time, it becomes debilitating: Alzheimer’s disease is the sixth most common cause of death in the United States according to the Alzheimer’s Association. But researchers still aren’t sure what causes it—let alone how to treat it.
A groundbreaking new study by a coalition of American scientists offers more definitive evidence than any past study that Alzheimer’s disease is somehow connected to viruses. But story headlines have largely focused on the two viruses the researchers found in greatest quantity: human herpesvirus (HHV) 6A and HHV 7. While they might be connected to the degenerative brain disease, they’re far from the only viruses the researchers studied—and unlike their better-known cousins HSV 1 and HSV 2, they aren’t sexually transmitted.
What the headlines are saying
“Herpes virus may play role in Alzheimer’s, study says.” “Alzheimer’s link to herpes virus in brain, say scientists.” “Researchers find herpes viruses in brains marked by Alzheimer’s Disease.” None of these headlines (which come from reputable news organizations) are technically incorrect, but they are misleading—especially the first two.
When most people hear herpes, they think HSV-1 and HSV-2—stigmatized, often sexually transmitted infections that have been unfairly linked in the popular press to health concerns like autism, unlikely methods of transmission like sample lipsticks, and in the past even Alzheimer’s. This last example might be where the current headlines are drawing their fear mongering, but the 2016 story that seemed to draw a link between the two was about nothing more than an editorial in the Journal of Alzheimer’s Disease that talked about the still-controversial idea that microbes such as viruses and bacteria might have something to do with causing Alzheimer’s. Most researchers who link these two things believe that microbial infections might trigger an immune response that helps explain why brain cells degenerate in Alzheimer’s patients. It is true that some studies point to a link between neurodegenerative diseases and autoimmune responses, where the body attacks itself, but that link is far from proven in the case of Alzheimer’s.
Two years later, there’s still no proof of a causative link between Alzheimer’s and any microbe, but this new study offers further evidence to support the idea that Alzheimer’s could have something to do with viruses and bacterial infections.
What the study actually says
Published in the journal Neuron, the new study gives the results of a large-scale analysis of data from the post-mortem brain samples of Alzheimer’s patients and “control” patients with normal brain function. They relied on four large databases of samples, which each contained multiple kinds of genetic information.
The researchers, who were actually looking for new brain-related genes to focus on for Alzheimer’s drug research, built computer models and ran their massive amount of data through them. When they looked at their preliminary results, says study author Joel Dudley of the Icahn School of Medicine at Mount Sinai, they saw that a number of the genes that seemed to be changing in the brains of Alzheimer’s patients were “known to have antiviral or antimicrobial activities.”
Chasing this unexpected finding, the researchers looked for genes from any virus, finding the greatest quantity of genes from HHV-6A and HHV-7, two incredibly common and closely related herpesviruses that are known to cause childhood rashes and fevers (there are nine known types of human-infecting herpesviruses, including the microbe that causes chicken pox). HHV-7 infection rates are thought to be close to 100 percent; that is to say, almost everyone carries these microbes. And while HHV-6A rates are unknown, due to the difficulty in distinguishing it from closely-related viruses, just about everyone has some form of HHV-6.
They also found plenty of other viral DNA, Dudley says, and the amount of HHV wasn’t dramatically higher than for other viruses. DNA from HSV-1 and HSV-2 was also present in comparatively high quantities, although less so than the other herpes strains.
What it actually means for the future of Alzheimer’s research
It’s not clear how these two poorly understood members the human herpesvirus family are transmitted, Dudley says, and the herpes finding isn’t the big takeaway from the study. For concerned members of the public—who probably carry HHV-6A and/or HHV-7, because it’s so common—he says there’s nothing to worry about. You certainly can’t change anything about your likelihood of getting Alzheimer’s disease by, say, injecting yourself with untested herpes treatments.
In fact, Dudley says, the findings are pretty hopeful. The study provides new evidence that “innate immune function somehow has a role in Alzheimer’s,” which could help researchers learn how to detect it earlier and treat it. “I do think the evidence is continuing to build that infectious agents play a role in this disease,” neurobiologist George Perry told Stat in their story about this new study.
Stat’s headline for the lengthy piece? “New study supports long-dismissed idea: Herpes viruses could play a role in Alzheimer’s.” A role—that’s all. We don’t know what role. So, once again, if you get a cold sore, don’t freak out.
Correction: A previous version of this article stated that infection rates of HHV-6 and -7 are close to 100 percent. Not all types of HHV-6 are confirmed to have this prevalence.
