SEOUL, South Korea: Scientists in South Korea have found strong evidence suggesting that harmful bacteria in the mouth may travel to the gut, influence brain activity, and potentially contribute to the development of Parkinson’s disease.
Parkinson’s disease is a common neurological disorder characterized by tremors, muscle rigidity, and slowed movement.
It affects an estimated 1–2 percent of people over the age of 65 and is among the most prevalent age-related brain disorders worldwide.
Previous studies had shown that the gut microbiome of individuals with Parkinson’s differs from that of healthy people, but the specific microbes involved and the mechanisms behind their impact were unclear. The new research helps bridge that gap.
The study found that people with Parkinson’s disease had unusually high levels of Streptococcus mutans—a bacterium best known for causing tooth decay—present in their gut microbiomes.
Once entered in the gut, this bacterium produces an enzyme called urocanate reductase (UrdA) and a metabolic compound known as imidazole propionate (ImP).
Researchers observed elevated levels of ImP in both the gut and bloodstream of Parkinson’s patients.
Evidence suggests that ImP can travel through the bloodstream to the brain, where it may contribute to the degeneration of dopamine-producing neurons, a defining feature of Parkinson’s disease.
The research was conducted by a multidisciplinary team led by Professor Ara Koh and doctoral researcher Hyunji Park from POSTECH’s Department of Life Sciences, in collaboration with experts from Sungkyunkwan University School of Medicine and Seoul National University College of Medicine.
Their findings were recently published in the journal Nature Communications.
To further investigate the link, scientists used mouse models in which S. mutans was introduced into the gut, or E. coli bacteria were genetically modified to produce UrdA.
These mice developed increased levels of ImP in their blood and brain tissue and displayed key Parkinson’s-like symptoms, including loss of dopamine-producing neurons, increased brain inflammation, impaired movement, and greater accumulation of alpha-synuclein, a protein associated with disease progression.
Additional experiments revealed that these harmful effects were driven by activation of the mTORC1 signaling pathway.
When mice were treated with an mTORC1 inhibitor, researchers observed significant reductions in neuroinflammation, neuronal damage, protein aggregation, and motor impairment.
The findings suggest that targeting harmful oral bacteria, their migration to the gut, or the metabolic byproducts they produce could open new avenues for preventing or treating Parkinson’s disease.
The study highlights the growing importance of oral and gut health in understanding complex neurological conditions.
