Could Common Germs Be Tied to Alzheimer’s?
Alzheimer’s Disease Symptoms, Risk, Treatment
Close to 6 million Americans now have Alzheimer’s disease. By 2050, that number likely will more than double. The fatal brain disease can’t yet be effectively treated or cured, but recent studies suggest that theory long on the fringes of Alzheimer’s research may provide new approaches to the disease.
Could common infections contribute to its development? “Scientists are really trying to pin that question down,” says Rebecca Edelmayer, PhD and director of scientific engagement at the Alzheimer's Association. Alzheimer's is a slowly progressive disease of the brain.
It’s a type of dementia. Harvard neurobiologist Robert Moir, PhD, does not believe that a single germ causes Alzheimer’s. Instead, he says it’s more likely that an infection in the brain could trigger a process that, in some people, results in the disease.
"The idea that infection could be connected to Alzheimer’s has been around for more than 100 years", says Moir, an assistant professor of neurology at both Harvard Medical School and Massachusetts General Hospital.
However, the idea fell by the wayside in the 1980s when most researchers turned their attention to a protein found in the brains of people with the disease. Called amyloid-beta, it has since been considered a prime suspect in the development of Alzheimer’s.
As Alzheimer’s progresses, amyloid-beta proteins build up in parts of the brain. They clump together to form hardened plaques that disrupt the way the brain functions. This leads to memory loss and other devastating Alzheimer’s symptoms. What’s unclear is why this buildup occurs. Amyloid-beta has been seen as “evil, bad, and an accident of metabolism” that serves no purpose, says Moir. He thinks that’s wrong.
Consider evolution, he says. Scientists have traced the same amyloid-beta that’s found in human brains back about 450 million years. It’s also present in most other vertebrates, including reptiles, birds, and fish. For something so ancient to remain unchanged for so long, says Moir, it must have a function. “What we did was look at what that function may be,” he says.
Here’s what he and his fellow researchers discovered: When a microbe, or infection, enters the brain, amyloid-beta goes on the attack. These tiny fibers wrap around the infection, forming into a ball of plaque that neutralizes the intruding germ. “The microbe is forever trapped,” says Moir.
“Amyloid-beta is not junk or functionless.” He and his colleagues observed this protective action in response to two common forms of the herpes virus for a study they published in the journal Neuron last summer. They found that they could trigger the development of amyloid plaques by injecting mice with the herpes virus. The same thing occurred in human brain cells in the lab.
For another study published in the same issue, a different team of researchers also investigated the link between herpes and Alzheimer’s. They found several types of the herpes virus in brain regions affected by Alzheimer’s. The viruses also appeared to influence the behavior of genes linked to amyloid-beta.
The World Health Organization estimates that two-thirds of the world’s population has a type of herpes studied by Moir and his team, known as HSV1. The other herpes virus they looked at is even more widespread. And once infected with herpes, you have it for life.
The question then becomes, if herpes is so common, why don’t more people develop Alzheimer’s? In most people, herpes causes no symptoms, because the virus remains inactive. Moir speculates that a combination of factors like age and genetics could activate the virus and trigger an inflammatory immune response in the brain that potentially leads to Alzheimer’s. “Perhaps there’s a mutation that prevents a gene from switching off that inflammation,” says Moir.
And there’s some research to suggest that treating herpes could reduce the risk of dementia. Taiwanese researchers found that over 10 years, HSV1 more than doubled the risk of dementia. However, people with the herpes virus who had been treated with an antiviral medication had the same risk as people who had never been infected.
Could treating herpes truly lower the chances of developing Alzheimer’s? The authors of the study say it’s too soon to tell. In 2016, a group of scientists from around the world published a joint statement in the Journal of Alzheimer’s Disease that called for more research into the connection between Alzheimer’s and infection. They noted that previous studies had suggested possible ties to infections such as the sexually transmitted disease chlamydia, fungal infections, and spirochetes, a type of bacteria that causes Lyme disease, syphilis, and other serious illnesses. Herpes, they point out, was first investigated nearly 30 years ago.
Nevertheless, the pursuit of the link between Alzheimer’s and infection has been embraced by only a handful of researchers, says Moir. And not all of them specialize in treating the brain.