Could harmful bacteria lurking in your mouth be a key player in the onset of Parkinson's disease? Recent findings from researchers in South Korea shed light on this intriguing connection, suggesting that these oral microbes might migrate to the gut and subsequently affect brain cells, thereby playing a pivotal role in the disease's development.
This groundbreaking study was spearheaded by Professor Ara Koh and doctoral student Hyunji Park from the Department of Life Sciences at POSTECH. Their research unveiled a biological mechanism revealing how substances produced by oral bacteria in the gut could initiate the processes leading to Parkinson's disease. The comprehensive results of their investigation were published in the esteemed journal Nature Communications. (https://www.nature.com/articles/s41467-025-63473-4)
One of the key discoveries made by the team was the increased presence of Streptococcus mutans within the gut microbiomes of individuals diagnosed with Parkinson's disease. This particular bacterium is known for producing an enzyme called urocanate reductase (UrdA) as well as a metabolic byproduct referred to as imidazole propionate (ImP). Both of these substances were found in elevated levels in the guts and bloodstreams of the affected patients. It appears that ImP has the ability to travel throughout the body, eventually reaching the brain and contributing to the degeneration of dopamine-producing neurons, which are crucial for coordinating movement and maintaining balance.
To delve deeper into this intriguing phenomenon, the research team conducted experiments involving mice. They either introduced S. mutans directly into the intestinal tracts of the mice or genetically engineered E. coli to produce UrdA. In both experimental setups, researchers noted a rise in ImP levels within the blood and brain tissues of the mice. Consequently, the rodents exhibited significant characteristics associated with Parkinson's disease, including damage to dopaminergic neurons, heightened brain inflammation, mobility issues, and an accumulation of alpha-synuclein—a protein closely linked to the progression of Parkinson's.
Further investigations revealed that the detrimental effects observed were closely tied to the activation of a signaling protein complex known as mTORC1. Remarkably, when the mice were treated with a drug designed to inhibit mTORC1, there was a notable decrease in brain inflammation, neuronal loss, alpha-synuclein buildup, and motor dysfunction. These promising results indicate that by targeting the oral-gut microbiome along with the compounds it generates, new therapeutic avenues may emerge for the treatment of Parkinson's disease.
