Amyloid beta protects against these viruses by latching onto them in large numbers, imprisoning them in self-assembling cages. That’s typically a good thing, but Moir argues that if the process goes on for too long, it builds up to the problematic plaques of Alzheimer’s. According to him, amyloid beta is still at the heart of the Alzheimer’s story, but it isn’t the villain. “In our model, Alzheimer’s is caused by amyloid beta’s reaction to something else, and most likely some kind of infection” like herpes, he says.

Moir notes that amyloid beta also exists in most other backboned animals. The protein first evolved around 400 million years ago, which is also roughly when the herpes virus family first appeared on the scene. “It’s clear that herpes and amyloid beta have been slugging it out since before there were insects,” Moir says. “One’s tuned to escape and the other to capture.”

This gives credence to the long-dismissed idea that viruses—and herpes, in particular—are involved in Alzheimer’s in some way. That’s not to say that the disease is contagious, nor that everyone with herpes infections is at risk. After all, HSV–1 and HHV–6 are extremely common. Two in three people have been infected by the former, which mostly causes cold sores. Almost everyone has encountered the latter.

In the past three decades, more than 100 papers have described correlations between the presence of HSV–1 and the risk of Alzheimer’s. Ruth Itzhaki from the University of Manchester notes that “hostility or derision occurred with most of my papers on this topic, and many people simply ignored them.” But evidence continues to grow. Most recently, Ben Readhead and his colleagues at the Icahn School of Medicine at Mount Sinai showed that two herpes viruses, HHV–6A and HHV–7, were more common in the brains of Alzheimer’s patients than in those of healthy people. The team confirmed this in three separate groups of patients. And they found that the more abundant the viruses, the worse the patients’ symptoms.

It’s possible that these herpes viruses are mere hitchhikers that are more likely to infect brains that are already deteriorating. But Readhead also showed that they can influence the activity of many human genes, including an unexpectedly large number that affect the risk of Alzheimer’s and the progression of the disease. “Some of these viruses are interacting with genes that are in the middle of known Alzheimer’s biology,” he says.

For example, the most infamous Alzheimer’s-related gene is ApoE. It comes in three forms, and the E4 version is the problem. People with one E4 copy have a threefold-higher risk of Alzheimer’s than those who have no copies, and those with two E4 copies have up to a twelvefold-higher risk. Readhead and his colleagues have shown that the more E4 copies someone has, the more HHV–6A and HHV–6B viruses they are likely to have in their brains.