Scientists Find Link Between Oral Bacteria and Parkinson’s Disease
Recent research has identified a connection between oral bacteria and Parkinson’s disease. It turns out that **Streptococcus mutans**, which is typically associated with tooth decay, can migrate to the gut and release compounds that affect the brain.
These compounds contribute to neuronal damage, inflammation, and movement difficulties that are characteristic of Parkinson’s disease. This discovery points toward the potential for targeting the oral and gut microbiome as a new approach to prevent or treat this condition.
Key Insights
- Oral-Gut-Brain Connection: **Streptococcus mutans** can move from the mouth to the gut, impacting the brain.
- Harmful Metabolite: Its metabolite, ImP, is harmful to dopamine-producing neurons and could worsen Parkinson’s symptoms.
- Potential Treatments: Inhibiting mTORC1 signaling led to reduced inflammation and motor issues in mice.
This new finding emphasizes the importance of maintaining good oral hygiene. Researchers from POSTECH and Sungkyunkwan University, along with colleagues from Seoul National University, conducted the study that unveiled how oral bacteria could potentially trigger Parkinson’s disease.
Their work illuminates the mechanism through which metabolites resulting from oral bacteria might lead to the development of the disorder.
The study was published online on September 5 in Nature Communications.
Parkinson’s disease is a serious neurological condition marked by tremors, muscle stiffness, and slowed movements. It affects about 1-2% of people over 65 globally, ranking it among the most prevalent age-related brain diseases.
While there have been earlier studies suggesting differences in gut microbiota between healthy individuals and those with Parkinson’s, the specifics regarding which microbes and metabolites are involved were less clear.
The researchers discovered that **Streptococcus mutans** is significantly more abundant in the gut microbiomes of individuals with Parkinson’s.
More importantly, **S. mutans** produces an enzyme called urocanate reductase (UrdA) along with its metabolite imidazole propionate (ImP). Both of these were found at higher levels in the guts and bloodstream of patients. It’s noteworthy that ImP seems to circulate within the body, reaching the brain and contributing to the degradation of dopamine neurons.
In experiments with mice, the team introduced **S. mutans** into their guts or engineered **E. coli** to produce UrdA. This led to increased ImP levels in both blood and brain tissues in the mice, along with symptoms typical of Parkinson’s disease: the loss of dopamine-producing neurons, increased neuroinflammation, motor function impairments, and higher aggregation of alpha-synuclein, a protein linked to the disease.
Further research indicated that these effects relate to the activation of a protein complex known as mTORC1. When the researchers treated the mice with an mTORC1 inhibitor, they observed a significant decrease in neuroinflammation, neuronal loss, and other Parkinson’s symptoms.
This leads to the conclusion that targeting the oral-gut microbiome and its metabolites might provide new ways to either prevent or treat Parkinson’s disease.
Professor Ara Koh remarked, “Our study helps clarify how oral microbes in the gut can impact the brain and be involved in the onset of Parkinson’s disease.” This suggests a fresh avenue for therapeutic approaches aimed at modifying gut microbiota in Parkinson’s treatment.
Funding: The research received support from various organizations, including Samsung Electronics and the Ministry of Science and ICT.
