A research team at Ajou University School of Medicine has proposed a new biological route connecting gut bacteria to the nerve cell damage seen in Parkinson's disease, according to 재활뉴스. The group, led by Lee Eun-jung of the Department of Brain Science and Park Dong-kyu of the Department of Neurology, points to a gene called hns in gut-dwelling E. coli and to a metabolite known as methylglyoxal (MG) as factors that can influence the expression of genes tied to nerve cell function. The findings were reported by 재활뉴스 and several Korean health outlets on November 3, 2026.
Parkinson's is a degenerative neurological condition in which dopamine-producing neurons in the brain progressively die off. While a growing body of research has suggested that gut microorganisms play some role in the disease, it has remained unclear which bacterial genes and substances actually reach or affect brain neurons.
Why it matters
The study offers a concrete molecular chain rather than a general correlation. If the pathway holds up in further work, it could sharpen the search for biomarkers — measurable signals that identify patients early or distinguish subtypes of the disease — and for targets that might one day be modulated therapeutically. The team's approach, which combines patient samples with experiments in worms and mice, is also notable for spanning several levels of evidence in a single paper.
The researchers stress that direct causation in humans and any clinical use remain open questions requiring more study.
What the patient samples showed
The team began by analyzing stool from Parkinson's patients. In the group whose disease is believed to begin with pathological changes in the body — including the gut — before reaching the brain, a subtype known as body-first Parkinson's, the E. coli hns gene appeared in relatively greater abundance.
A separate analysis of patient blood found that this same body-first group carried higher concentrations of methylglyoxal than patients whose disease appears to start in the brain. MG is produced during metabolic processes in both bacteria and the human body, and can harm cells when it accumulates beyond normal levels.
Worm and mouse experiments
To test whether these two factors actually affect neurons, the team turned to a nematode model of Parkinson's disease. When the worms were fed E. coli that had the hns gene — which is involved in MG production — removed, damage to dopamine neurons declined. When MG was added back, that protective effect disappeared. According to the reporting, this indicates that the bacterial gene and the metabolite can both influence dopamine neuron damage.
Further analysis identified a gene called rig-5 as involved in the nerve cell protection seen in the worms. That led the researchers to LSAMP, a human gene thought to play a comparable role and known to be involved in neuron function and in the connections between nerve cells.
In human neurons exposed to MG, LSAMP expression fell. Brain tissue from Parkinson's patients likewise showed lower expression of the gene. In mice colonized in the gut with E. coli lacking hns, by contrast, LSAMP expression rose.
What the team says
Lee Eun-jung said the work's significance lies in proposing a new connecting pathway through which a specific gut E. coli gene and a metabolite can affect gene expression in nerve cells, according to 재활뉴스. She added that the team plans follow-up research to clarify the relationship between gut microbes and Parkinson's in greater detail.
The study's contribution, as the team frames it, is a proposed link — hns and MG on one side, rig-5 and LSAMP on the other — supported by patient data and multiple experimental models rather than a demonstrated cause of the disease in people.
Watch for follow-up work testing whether the same pathway operates in human patients over time, and whether MG or LSAMP can be measured reliably enough to serve as clinical markers.
