A study published in 2019 raised significant interest by suggesting a possible link between Alzheimer’s disease and gum disease. The research, led by microbiologist Jan Potempa from the University of Louisville, found traces of Porphyromonas gingivalis—the bacterium responsible for chronic periodontitis—in the brains of individuals who had died with Alzheimer’s.

Earlier experiments conducted by the biotechnology company Cortexyme provided further insight. In animal studies, mice that were orally infected with P. gingivalis showed increased production of beta-amyloid, the sticky protein widely associated with Alzheimer’s disease. This finding strengthened the theory that oral bacteria could influence changes in the brain linked to cognitive decline.

Scientists have long suspected that infections might contribute to Alzheimer’s development, but clear evidence of causation has been difficult to establish. As Dr. Stephen Dominy, co-founder of Cortexyme, explained, infectious agents have been considered before, yet proof strong enough to confirm a direct cause has remained limited.

The researchers focused on gingipains—harmful enzymes produced by P. gingivalis. High levels of these toxins were found to be associated with tau and ubiquitin, two proteins already known to play a role in Alzheimer’s pathology. This connection suggested a potential biological pathway through which the bacteria might contribute to brain damage.

However, gingipains were also detected in the brains of individuals who had never been formally diagnosed with Alzheimer’s. This raised an important question: did these individuals develop early disease without symptoms, or did Alzheimer’s-related cognitive decline later lead to poor oral hygiene? The researchers argue that the presence of gingipains in people without dementia suggests the infection may occur before noticeable cognitive decline, rather than being a consequence of it.

Further experiments in mice showed promising results when researchers used a compound known as COR388. This treatment reduced amyloid-beta levels and brain inflammation in the animals. While these findings are encouraging, scientists caution that results seen in mice do not always translate directly to humans.

As Alzheimer’s Research chief scientific officer David Reynolds noted, no new dementia treatments have been introduced in over 15 years. For that reason, exploring novel approaches—such as targeting bacterial toxins—is considered essential, even though human studies are still needed to confirm effectiveness and safety.