Short chain fatty acids and gut microbiota differ between patients with Parkinson’s disease and age-matched controls Original paper

What was studied?

This original study examined Parkinson’s disease gut microbiome signatures, focusing on whether specific microbial shifts and reduced short-chain fatty acid (SCFA) production are characteristic of Parkinson’s disease (PD). The researchers quantified fecal SCFAs—acetate, propionate, and butyrate—and profiled key bacterial phyla and taxa by quantitative PCR. They aimed to determine whether well-documented gastrointestinal dysfunction in PD corresponds to measurable microbial and metabolic alterations. This question matters because PD pathology affects the enteric nervous system early, and gut-related mechanisms are increasingly suspected to influence disease onset or progression. By comparing PD patients to age-matched controls, the investigators sought to clarify whether changes in the microbiome and microbial metabolites could be linked to PD-related dysmotility or broader neurodegenerative processes.

Who was studied

The study included 34 individuals diagnosed with Parkinson’s disease, all on dopaminergic medication and following an omnivorous diet without recent antibiotic, probiotic, or prebiotic exposure. Their samples were compared with those from 34 age-matched healthy controls without gastrointestinal disease or medications affecting motility. An additional group of 10 younger controls was included to contextualize age-related differences. PD participants had a mean age of 67.7 years and a median Hoehn and Yahr stage of 2.5. Constipation was reported by seven PD participants, while only two controls noted similar symptoms. These carefully curated groups allowed the authors to isolate disease-related microbial patterns from potential confounders such as age or diet.

Most important findings

PD patients demonstrated substantially reduced fecal concentrations of acetate, propionate, and butyrate, including significantly lower relative butyrate levels. These deficits exceeded typical age-related declines. Microbiome composition showed clear shifts: Bacteroidetes and Prevotellaceae were reduced, while Enterobacteriaceae and Bifidobacterium were increased. Within the Firmicutes phylum, the butyrate-producer Faecalibacterium prausnitzii was markedly reduced, alongside Lactobacillaceae and Enterococcaceae. Elevated Enterobacteriaceae in PD were consistent across clinical phenotypes. The study also noted correlations between entacapone use and lower Firmicutes abundance and butyrate levels, hinting at medication-microbiota interactions. Altogether, the microbial profile reflects reduced beneficial taxa, increased potentially pro-inflammatory Proteobacteria, and impaired SCFA metabolic output.

Key implications

These findings suggest that PD is associated with a recognizable gut microbiome signature marked by reduced SCFA production and depletion of key butyrate-producing bacteria. This pattern may compromise epithelial barrier integrity and influence enteric nervous system function, potentially contributing to constipation and early gut-related pathology in PD. Although causality cannot be determined, the convergence of microbial dysbiosis and metabolic impairment strengthens hypotheses that gut-brain interactions play a role in PD development. Future longitudinal and mechanistic studies are needed to determine whether modifying the gut ecosystem could have therapeutic or preventative relevance.

Citation

Unger MM, Spiegel J, Dillmann KU, et al. Short chain fatty acids and gut microbiota differ between patients with Parkinson’s disease and age-matched controls. Parkinsonism Relat Disord. 2016;32:66-72. doi:10.1016/j.parkreldis.2016.08.019