“We can’t make any causal inferences” from these studies, cautions Maria Carrillo, the chief scientific officer of the Alzheimer’s Association. “Their findings don’t prove the viruses lead to Alzheimer’s progression, but there is a relationship, and we need to understand what herpes viruses are doing in the brain.”
Moir suspects that as we get older, herpes viruses take advantage of our weakening immune systems to spread from other parts of the body into the brain. Amyloid beta rises to meet them in battle, and deposits of amyloid-entrapped viruses start to accumulate in the brain. This goes on for years, and slowly but surely leads to the other hallmarks of Alzheimer’s.
This is all conjecture for now. It’s also possible that herpes simply exacerbates a process of amyloid accumulation that has been triggered by something else, or that other changes in the brain allow long-standing herpes infections to run amok. “It’s going to be more complicated than a simple case of an infection leading to disease,” Moir says.
“These studies suggest a possible role of viral infection as a contributing factor to Alzheimer’s disease,” says Li-Huei Tsai, a neuroscientist at MIT who studies the disease. “But it remains to be seen if drugs used to treat herpes-virus infection can be protective against Alzheimer’s.”
Hints that they can already exist. One study published earlier this year tracked the health of about 78,000 Taiwanese people, half of whom had been diagnosed with shingles within a 16-year period. Shingles is caused by a herpes virus called VZV, which also causes chicken pox in children. Among adults, the study found that people with a recent shingles flare-up had an 11 percent higher risk of developing dementia than healthier peers. And strikingly, those who were treated with anti-herpes drugs had a 45 percent lower risk of developing dementia than their untreated peers.
A second Taiwanese study looked at more than 8,000 people who had been recently diagnosed with HSV–1. Over the next decade, those people were 2.5 times more likely to develop dementia than uninfected peers. But again, that risk fell by 80 percent among those who had been treated with anti-herpes drugs. “That’s perhaps the strongest epidemiological data to emerge so far,” Moir says.
These drugs would have to be tested in clinical trials. And even if they can reduce the risk of Alzheimer’s, “they aren’t very pleasant and you can’t treat everyone,” Moir says. “The problem is how do you find people who have a herpes infection that warrants targeting with medications? It’s not clear.”
Scientists have spent decades trying to develop treatments for Alzheimer’s by creating drugs that get rid of amyloid beta. This approach has been catastrophically unsuccessful, with hundreds of clinical trials and nothing to show for them. Perhaps a better understanding of what amyloid beta actually does, and how it interacts with viruses, could lead to better strategies for beating Alzheimer’s—a disease that affects almost 30 million people worldwide.
Ed Yong is a staff writer at
The Atlantic, where he covers science.