Dysbiosis of gut microbiota in a selected population of Parkinson’s patients Original paper

What was studied?

This study examined gut microbiota dysbiosis in Parkinson’s disease, focusing on whether specific microbial patterns could act as predictive markers of disease presence and severity. By analyzing the gut microbiota dysbiosis in Parkinson’s disease using 16S rRNA gene sequencing, the researchers sought to determine how bacterial families shifted between Parkinson’s disease (PD) patients and healthy controls, and how these shifts aligned with clinical phenotypes. The investigation explored how diet, lifestyle, age, sex, and weight changes influenced microbial composition, while also assessing microbial functional pathways, including short-chain fatty acid (SCFA) metabolism, amino acid biosynthesis, and lipopolysaccharide (LPS) production.

Who was studied?

The research evaluated 152 fecal samples derived from 80 carefully selected PD patients and 72 healthy controls residing in Central Italy. PD participants were enrolled using strict inclusion criteria to reduce heterogeneity, and detailed assessments of their lifestyle habits, dietary patterns, body mass index, and clinical motor scores (Hoehn & Yahr stage, MDS-UPDRS Part III) were performed. This enabled the researchers to account for confounders and identify predictors associated with microbial alterations. The cohort’s demographics and clinical features allowed for focused evaluation of microbiota-phenotype relationships, particularly those related to disease progression.

Most important findings

The gut microbiota of PD patients demonstrated a consistent dysbiosis characterized by higher levels of Lactobacillaceae, Enterobacteriaceae, and Enterococcaceae, along with a marked reduction in Lachnospiraceae. Because Lachnospiraceae include major SCFA-producing taxa, their depletion suggests impaired butyrate production, reduced epithelial integrity, and loss of anti-inflammatory regulation in the gut. Conversely, enriched Enterobacteriaceae and Enterococcaceae are known contributors to LPS biosynthesis, which intensifies pro-inflammatory signaling.

Lower Lachnospiraceae and elevated Enterobacteriaceae correlated directly with more severe motor impairment—strongly linking microbial imbalance to clinical phenotype. Predictive metagenomics further showed diminished pathways for SCFA and amino acid biosynthesis, including precursors for neurotransmitter synthesis, pointing to microbial contributions to PD-related neurotransmission deficits. Increased pathways related to LPS biosynthesis added evidence for a sustained pro-inflammatory gut milieu.

Key implications

The study reinforces the concept that Parkinson’s disease is associated with a gut-driven inflammatory signature. The reduction of SCFA-producing bacteria and increased abundance of LPS-producing families present a biologically plausible mechanism linking intestinal dysbiosis to neuroinflammation and motor symptom severity. These findings underscore the microbiome’s relevance as both a potential biomarker and a therapeutic target. Though not yet definitive enough for clinical diagnostics, the consistent shifts observed help narrow candidate microbial signatures for future clinical integration and microbiome-based interventions. This research strengthens the rationale for monitoring gut microbiota dysbiosis in Parkinson’s disease as part of personalized care strategies and contributes valuable microbial associations for microbiome signatures databases.

Citation

Pietrucci D, Cerroni R, Unida V, et al. Dysbiosis of gut microbiota in a selected population of Parkinson’s patients. Parkinsonism Relat Disord. 2019;65:124-130. doi:10.1016/j.parkreldis.2019.06.003