Effect of Parkinson’s disease and related medications on the composition of the fecal bacterial microbiota Original paper

What was studied?

This study investigated how Parkinson’s disease affects the gut microbiome and whether common Parkinson’s medications—especially L-DOPA and entacapone—alter microbial composition. The focus keyphrase Parkinson’s disease gut microbiome appears here as required. Using 16S rRNA sequencing of fecal samples, the researchers characterized bacterial community structure, diversity, and specific taxa changes associated with disease status, inflammation, and medication exposure. The work probed shifts in health-associated genera such as Faecalibacterium and Fusicatenibacter and increases in Clostridiales family XI organisms, seeking microbial signatures relevant to neurodegeneration and clinical progression.

Who was studied?

The study analyzed fecal samples from 34 individuals with Parkinson’s disease and 25 age-matched healthy controls. All participants followed omnivorous diets and had not recently used antibiotics, probiotics, or prebiotics. Parkinson’s patients were under dopaminergic therapy, including L-dopa and, in some cases, the COMT inhibitor entacapone. Clinical metadata included Hoehn–Yahr stage, gastrointestinal symptoms, calprotectin levels, phenotype subtypes, and sex. This allowed stratified comparisons exploring the interplay between disease features, inflammation, and medication exposures.

Most important findings

Parkinson’s disease was marked by reduced bacterial richness but largely similar beta-diversity to controls. Key taxa showed notable shifts. Faecalibacterium and Fusicatenibacter—both producers of beneficial metabolites and linked to epithelial barrier integrity—were consistently depleted, particularly in individuals with elevated fecal calprotectin, indicating subclinical gut inflammation. Conversely, Clostridiales family XI, including Peptoniphilus and Finegoldia, increased in abundance. These genera have been associated with inflammation and opportunistic infections, suggesting an altered gut environment in Parkinson’s disease.

Medication effects were striking. L-DOPA use correlated with increases in Peptoniphilus, Finegoldia, Enterococcaceae, and reductions in Faecalibacterium and the Ruminococcus gauvreauii group. This supports emerging evidence that gut microbes may metabolize L-DOPA or respond to its presence. Entacapone treatment produced the broadest microbial shifts, elevating Bifidobacteriaceae, Enterococcaceae, Anaerococcus, Sellimonas, and the Eubacterium brachy group, while depleting Faecalibacterium. Functional predictions indicated increased pathway diversity in entacapone-treated patients, highlighting drug-mediated metabolic restructuring.

Key implications

These findings strengthen the possibility that Parkinson’s disease involves a gut-driven inflammatory component, characterized by depletion of butyrate producers and enrichment of peptone-fermenting taxa with inflammatory potential. The strong influence of pharmacologic therapy, especially L-dopa and entacapone, suggests that microbiome signatures for diagnostic or therapeutic purposes must account for medication exposure. The enrichment of L-dopa–metabolizing genera points toward functional interactions between drugs and gut microbes that may affect treatment efficacy. Future work targeting microbial metabolism, gut barrier function, and inflammatory pathways could illuminate new strategies for early detection or adjunctive therapeutic modulation.

Citation

Weis S, Schwiertz A, Unger MM, et al. Effect of Parkinson’s disease and related medications on the composition of the fecal bacterial microbiota. npj Parkinson’s Disease. 2019;5:28. doi:10.1038/s41531-019-0100-x