Tooth Decay & Parkinson’s: Brain Health Link Revealed

Parkinson’s disease is a neurodegenerative disease that can cause hand tremors, muscle stiffness, decreased balance, and eventually the gradual loss of self-care ability. Since there is no complete cure, how to avoid the disease is even more important. Recently, Pohang University of Science & Technology in South Korea discovered that oral bacteria closely related to tooth decay may be involved in the development of Parkinson’s disease. This discovery provides a new perspective on the prevention of Parkinson’s disease. The paper was recently published in the journal “Nature Communications”.

Streptococcus mutans is the key bacterium that causes tooth decay. It forms dental plaque on the tooth surface and produces acidic metabolites that erode enamel. When analyzing the intestinal microbiota of patients with Parkinson’s disease, the team unexpectedly discovered that the proportion of this bacteria, which originally belonged to the oral cavity, increased significantly in the patients’ intestines, indicating that Streptococcus transsaccharides can not only survive in the intestines, but may also participate in the intestinal metabolic network.

Key metabolite: imidazole propionic acid

Further analysis showed that the intestinal tract of transsaccharic Streptococcus produces a small molecule metabolite called imidazole propionate. Past studies have linked imidazole propionate to metabolic abnormalities, but less is known about its effects on the nervous system. In addition, the enzyme “urocanate reductase” responsible for producing imidazole propionic acid has higher levels in the intestines and blood of patients with Parkinson’s disease, indicating that these metabolites may accumulate in the patient’s body and affect the whole body and nervous system.

During animal experiments, the team implanted Streptococcus transsaccharides into the intestines of mice. The results showed that as long as imidazole propionic acid accumulates, mice will develop brain lesions similar to Parkinson’s disease, such as nerve cell damage, chronic inflammation, and abnormal protein accumulation in nerve cells. In addition, mice also develop significant motor dysfunction. Changes in intestinal metabolism have been shown to be sufficient to affect the health of the nervous system.

mTORC1: A key link between the colon and neurodegeneration

Molecular-level studies have shown that imidazole propionic acid stimulates protein synthesis signals in nerve cells, leading to abnormal protein structure and thus promoting inflammatory responses. When the research team used drugs to inhibit the key signaling protein mTORC1, neuropathy and movement disorders were alleviated, indicating that mTORC1 may be an important hub in the conversion of intestinal metabolic signals into brain lesions.

Overall, this study adds to the new understanding that risk factors for Parkinson’s disease may not just be due to aging or genetics, but also to the activity of bacteria in the mouth and gut. Although it is still not possible to directly equate tooth decay with Parkinson’s disease, the long-term effects of intestinal metabolites on the nervous system must be taken seriously. In the future, focusing on oral health care and intestinal microbiota may provide more possibilities for Parkinson’s disease prevention.

(First image source: Unsplash)