Structural changes of gut microbiota in Parkinson’s disease and its correlation with clinical features Original paper

What was studied?

The study investigated gut microbiota in Parkinson’s disease, examining structural differences between patients with Parkinson’s disease (PD) and healthy controls while correlating microbial patterns with clinical features. Using 16S rRNA sequencing, the researchers characterized fecal bacterial communities and assessed how microbial shifts aligned with PD severity, duration, and non-motor symptoms. This work explored whether reductions in beneficial short-chain–fatty-acid–producing taxa and increases in potential pathobionts represented a biologically meaningful microbial signature of PD, potentially shaping inflammation, gut–brain interactions, and neurodegenerative processes. Findings were interpreted in the context of α-synuclein pathology and gastrointestinal symptoms that often precede motor manifestations.

Who was studied?

The study included 24 PD patients and 14 age- and gender-matched healthy controls recruited in Beijing. PD diagnosis followed the UK Brain Bank Criteria, and subjects were excluded if recent antibiotic or probiotic use, gastrointestinal disease, or unstable medical conditions were present. Nearly all PD participants were on antiparkinsonian medication. Clinical data included Unified Parkinson Disease Rating Scale (UPDRS), Hoehn & Yahr staging, constipation scoring, and ratings for anxiety, depression, and non-motor symptoms. Subgroup analyses compared mild PD (Hoehn & Yahr 1–2.5) with severe PD (3–5), allowing assessment of stage-dependent microbial patterns.

Most important findings

Across phylum, family, and genus levels, PD microbiota showed distinct structural deviations from controls. A central pattern was the loss of putative cellulose-degrading, short-chain–fatty-acid–producing genera—Faecalibacterium, Blautia, and Ruminococcus—all significantly reduced in PD. Conversely, potential pathobionts—Escherichia-Shigella, Proteus, Streptococcus, and Enterococcus—were enriched, suggesting increased inflammatory and neurotoxin-producing capacity. At the phylum level, PD subjects exhibited reduced Bacteroidetes and elevated Actinobacteria and Proteobacteria.

Disease stage analyses showed a stepwise decline in Faecalibacterium from controls to mild PD to severe PD (5.14% → 3.17% → 1.22%), while Megasphaera rose progressively, hinting at dynamic microbial remodeling with disease progression. Correlation matrices and scatter plots demonstrated robust associations: UPDRS scores and PD duration positively correlated with Enterococcus, Proteus, and Escherichia-Shigella, and negatively correlated with Blautia, Ruminococcus, and Faecalibacterium. These relationships were independent of age, BMI, and gender.

Key implications

The findings suggest a microbiome signature in PD characterized by erosion of SCFA-producing taxa and expansion of endotoxin- and neurotoxin-producing species. Reduced SCFA production may compromise gut barrier integrity, amplify inflammation, and potentially enhance α-synuclein pathology in the enteric nervous system. Increased pathobionts may contribute to systemic inflammatory signaling relevant to neurodegeneration. These microbial shifts correlate with disease severity, reinforcing their potential as biomarkers. The results encourage future mechanistic studies, metagenomic functional profiling, and exploration of microbiome-targeted interventions such as probiotics or fecal microbiota transplantation.

Citation

Li W, Wu X, Hu X, et al. Structural changes of gut microbiota in Parkinson’s disease and its correlation with clinical features.Sci China Life Sci. 2017;60. doi:10.1007/s11427-016-9001-4