Oral bacteria that settle in the gut may produce chemicals that damage brain cells and play a role in Parkinson’s disease, researchers have suggested.
Scientists found that Streptococcus mutans – the bacterium responsible for tooth decay – was more common in the guts of Parkinson’s patients than in healthy people.
The finding adds to the case for good dental hygiene, as the study shows how cavity-causing microbes might contribute to a neurological condition affecting one to two per cent of people over 65.
Researchers identified how metabolites produced by these oral bacteria in the gut may trigger the disease’s development.
The team, led by professor Ara Koh and doctoral candidate Hyunji Park of POSTECH, with professor Yunjong Lee and doctoral candidate Jiwon Cheon of Sungkyunkwan University, collaborated with professor Han-Joon Kim of Seoul National University.
Professor Ara Koh said: “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.
It highlights the potential of targeting the gut microbiota as a therapeutic strategy, offering a new direction for Parkinson’s treatment.”
The researchers showed that S. mutans produces an enzyme called urocanate reductase (UrdA) and its metabolite imidazole propionate (ImP).
Both were found at higher levels in patients’ guts and blood.
ImP appeared able to enter the bloodstream, reach the brain and contribute to the loss of dopaminergic neurons – brain cells that make dopamine, which is vital for movement control.
In mouse studies, scientists introduced S. mutans into the gut or engineered E. coli to express UrdA.
The mice developed raised ImP levels in blood and brain tissue and signs typical of Parkinson’s: loss of dopaminergic neurons, increased inflammation, impaired movement and greater build-up of alpha-synuclein, a protein central to the disease.
Further experiments showed these effects depended on activation of a protein complex called mTORC1.
Treating mice with an mTORC1 inhibitor significantly reduced inflammation, neuron loss, alpha-synuclein build-up and movement problems.
