Korean researchers say this common bacterium's journey throughout the body could lead to consequences in the brain.
Parkinson’s disease, a progressive neurological disorder affecting more than 1.1 million people in the U.S, is characterized by tremors, stiffness, and slowed movement, according to the Parkinson’s Foundation. While the exact cause of most Parkinson’s cases currently remains unknown, emerging research hints that the gut-brain axis—the complex communication system between the digestive tract and the brain—may be an important piece of the puzzle.
Now, there’s evidence suggesting that a common culprit behind tooth decay may do more than harm your smile—it could also play a role in the development of Parkinson’s disease.
The September 2025 study, published in Nature Communications from researchers primarily at South Korea’s Pohang University of Science & Technology, found that Streptococcus mutans—a bacterium best known for causing cavities—can travel from the mouth to the gut, where it produces compounds that may damage brain cells involved in movement and coordination.
The basis for this research comes after another study confirmed through fecal sample analysis that individuals with Parkinson’s had higher levels of S. mutans in their gut microbiome compared with healthy individuals. This oral microbe can then produce an enzyme with a metabolic byproduct known as imidazole propionate (ImP). Imidazole propionate, in turn, “travel through the body, reach the brain, and contribute to the loss of dopamine-producing neurons,” per a news release.
The scientists, in hopes of better understanding this connection, conducted experiments in mice showed that when S. mutans or “genetically modified E. coli” were introduced directly into their guts, blood and brain levels of imidazole propionate rose. The animals then developed key features of Parkinson’s, including the loss of dopamine-producing neurons, increased inflammation in the brain, motor dysfunction, and accumulation of alpha-synuclein, a protein tied to Parkinson’s progression.
“Our study provides a mechanistic understanding of how oral microbes in the gut can influence the brain and contribute to the development of Parkinson’s disease,” said assistant professor of molecular medicine Ara Koh, a co-author of the study. “It highlights the potential of targeting the gut microbiota as a therapeutic strategy, offering a new direction for Parkinson’s treatment.”
Importantly, the researchers conducted additional experiments in the mice that showed the Parkinson-like effects depended on “activation of a signaling protein complex called mTORC1.” They found that when the mice were treated with a medication that inhibited mTORC1, their symptoms improved.
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