Alzheimer's Plaques Protect The Brain Against The Herpes Virus

When the herpes virus (orange) infects neurons (purple), beta-amyloid plaques form to protect the brain cells, but at the cost of Alzheimer's disease further down the track. Kateryna Kon/Shutterstock

Sometimes a scientific field appears to make little progress for years, before announcements come in a rush. At least to non-neuroscientists, that looks to be the case with the connection between the herpes virus and Alzheimer's disease. Just last month a paper reported that brain tissues from people with Alzheimer's are twice as likely to have been infected with two common strains of herpes as tissues from people without, and now we may know why.

Last month's research wasn't the first to suggest a link between herpes and dementia, although it was the most convincing. Now Dr Rudolph Tanzi of Massachusetts General Hospital has shown that beta-amyloid proteins, which form plaques in the brains of people with Alzheimer's disease, trap herpes virus particles, preventing immediate damage to the brain. Unfortunately, once the plaques have been “seeded” in response to the virus they keep growing, with disastrous consequences later on.

The work has focused on the HSV-1 virus, which predominantly causes cold sores, not the rarer but more famous HSV-2, which is associated with more frequent re-occurrences of genital infections.

Beta-amyloid plaques have been considered waste products with no useful purpose of their own. However, Tanzi and colleagues found that mice infected with HSV-1 survive significantly longer if they can express beta-amyloid than if they cannot.

Reporting in Neuron, the team showed that the protein binds to the virus and prevents it from attacking the brain, but at the cost of inducing plaques much earlier in the mice's lives than normal.

“Our findings reveal a simple and direct mechanism by which herpes infections trigger the deposition of brain amyloid as a defense response in the brain," Tanzi said in a statement. "In this way, we have merged the infection hypothesis and amyloid hypothesis into one ‘Antimicrobial Response Hypothesis’ of Alzheimer’s disease.” 

The work suggests that controlling Alzheimer's may not be as simple as targeting beta-amyloid, since its absence could lead to even swifter damage. On the other hand, if forthcoming trials of a herpes vaccine prove effective we may find it going some way to solving even bigger problems than the ones against which it was designed.

However, while herpes may be the most common infectious agent stimulating beta-amyloid growth, it's not unique. Tanzi and colleagues have previously shown the protein has a protective role against fungal and bacterial infections. Consequently, while a vaccine against, or treatment for, herpes might help reduce the number of Alzheimer's cases, we'll need something much more comprehensive to stop the disease entirely.

Tanzi is leading the “Brain Microbiome Project”, exploring the possibility that, like the gut, the brain normally has a population of beneficial microbes whose disruption makes way for pathogens to take over.

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