Brain infections may spark Alzheimer’s, new study suggests

While still speculative, new hypothesis offers some sensible explanations to the disease.

Beth Mole – May 30, 2016 5:00 pm | 51

The protein globs that jam brain circuits in people with Alzheimer’s disease may not result from a sloppy surplus, but rather a bacterial battle, a new study suggests.

Previously, researchers assumed that the protein—beta amyloid—was just a junk molecule that piled up. And efforts to cure Alzheimer’s focused on clearing out clogs and banishing beta amyloid from the brain. But a new study conducted using mice and worms suggests that the protein clumps are actually microbial booby traps, sturdy proteinaceous snares intended to confine invading microbes and protect the brain.

The findings, published in the journal Science Translational Medicine, suggest that Alzheimer’s may result from the brain’s effort to fight off infections. While that hypothesis is controversial and highly speculative at this point, it could dramatically alter the way researchers and doctors work to treat and prevent the degenerative disease.

The findings are “fascinating,” Colin Masters, a neuroscientist at the University of Melbourne in Australia, told Science. But because the study was carried out in mice and worms, the findings are “very contrived in the sense that they don’t bear a direct relationship to what we see in the human condition.”

Still, the findings have many scientists intrigued, and some say they make a lot of sense. For instance, past research had found that people who developed Alzheimer’s had increased levels of antibodies to herpes virus, suggesting past infections. But the idea that herpes caused Alzheimer’s seemed far-fetched, Michael Weiner, an Alzheimer’s disease neuroimaging researcher at the University of California, San Francisco, told the New York Times. He said that the new data provides a plausible explanation as well as being “interesting and provocative.”

In the study, researchers at Harvard injected a lethal dose of bacteria into the brains of mice genetically engineered to overproduce amyloid beta—a model for studying Alzheimer’s disease—as well as normal mice. Overnight, the Alzheimer’s model mice developed protein plaques similar to those seen in people with the disease. At the center of each plaque was a single bacterial cell. The control mice, on the other hand, didn’t form plaques and died faster.

In worms called Caenorhabditis elegans, another model organism, researchers saw similar results. Extra amyloid in the worms’ guts prolonged their life after infection with bacteria and yeast.

If the findings hold up in further studies, the data points to problems clearing out the infection debris in patients with Alzheimer’s and may provide hints to new treatments. Researchers are already starting new studies to follow-up on these results.

Science Translational Medicine, 2016. DOI: 10.1126/scitranslmed.aaf1059 (About DOIs).