How gum disease could lead to Alzheimer’s

Senior Living

By Maria Cohut
Fact checked by Carolyn Robertson

In a new study, researchers have found that a bacterium largely responsible for gum disease also contributes to the development of Alzheimer’s disease.

According to data from the National Institute of Dental and Craniofacial Research, 8.52 percent of adults between 20 and 64 years of age in the United States have periodontitis (gum disease).

Gum disease is a widespread problem that can lead to more negative outcomes, from tooth loss to an increased risk of cancer.

Now, emerging evidence suggests that one of the bacteria involved in periodontitis could also contribute to the accumulation of toxic proteins in the brain, which scientists have associated with the development of Alzheimer’s disease.

These findings have emerged from a new study in mice that researchers from Cortexyme, Inc., a pharmaceutical company that aims to develop new therapeutics for Alzheimer’s disease, have conducted.

The results of the research — whose lead author is Dr. Stephen Dominy, Cortexyme co-founder — appear in the journal Science Advances.

“Infectious agents have been implicated in the development and progression of Alzheimer’s disease before, but the evidence of causation hasn’t been convincing,” notes Dr. Dominy.

Senior Living
A bacterium involved in gum disease boosts Alzheimer's toxicity.

The bacterium that boosts brain toxicity

The researchers zeroed in on one bacterium — Porphyromonas gingivalis — which is a Gram-negative oral anaerobe that drives the development of gum disease.

  1. gingivalis, the researchers note, also appears in the brains of people who doctors have diagnosed with Alzheimer’s disease, which left the investigators intrigued.

When looking at a mouse model, the team found that infection with P. gingivalis led to greater production of beta-amyloid in the rodents’ brains.

Beta-amyloid is a marker of Alzheimer’s disease in the brain; in this neurodegenerative condition, the toxic protein accumulates in excess, forming into plaques that disrupt normal communication between brain cells.

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