Emerging research suggests that Alzheimer’s disease may be linked to an unexpected culprit — gum disease.

A study discovered the presence of Porphyromonas gingivalis, a bacteria responsible for chronic periodontitis, in the brains of deceased Alzheimer’s patients.

Researchers found that when mice were infected with the bacteria, it colonized their brains and triggered the production of amyloid beta, a protein commonly associated with Alzheimer’s. This evidence strengthens the hypothesis that the disease could have infectious origins rather than being solely a neurodegenerative disorder.

The study also revealed that toxic enzymes from the bacteria were present in individuals who had Alzheimer's-related brain changes but had not yet been diagnosed with dementia, suggesting the infection may begin years before symptoms appear.

This discovery opens the door to new potential treatments. A pharmaceutical company, Cortexyme, developed a compound called COR388, which showed promise in reducing both bacterial infection and amyloid beta accumulation in animal trials. While human trials are needed to confirm its effectiveness, the study underscores the importance of oral hygiene in brain health. Scientists remain cautiously optimistic, emphasizing that with no new dementia treatments in over 15 years, investigating all possible causes is crucial. While more research is needed, the link between gum disease and Alzheimer’s highlights a simple yet vital message: taking care of your teeth might help protect your brain in the long run.

Porphyromonas gingivalis, the keystone pathogen in chronic periodontitis, was identified in the brain of Alzheimer’s disease patients. Toxic proteases from the bacterium called gingipains were also identified in the brain of Alzheimer’s patients, and levels correlated with tau and ubiquitin pathology. Oral P. gingivalis infection in mice resulted in brain colonization and increased production of Aβ_1–42, a component of amyloid plaques. Further, gingipains were neurotoxic in vivo and in vitro, exerting detrimental effects on tau, a protein needed for normal neuronal function. To block this neurotoxicity, we designed and synthesized small-molecule inhibitors targeting gingipains. Gingipain inhibition reduced the bacterial load of an established P. gingivalis brain infection, blocked Aβ_1–42 production, reduced neuroinflammation, and rescued neurons in the hippocampus. These data suggest that gingipain inhibitors could be valuable for treating P. gingivalis brain colonization and neurodegeneration in Alzheimer’s disease.