Analysis of the Gut Microflora in Patients With Parkinson’s Disease Original paper

What was studied?

This original research article examined Parkinson’s disease gut microflora, characterizing fecal microbiome composition in Chinese patients with Parkinson’s disease (PD) to assess how disease stage and antiparkinsonian medications relate to microbial patterns. Using high-throughput Illumina MiSeq sequencing targeting the 16S rRNA gene, the authors compared operational taxonomic units, α-diversity, β-diversity, and taxonomic shifts between newly diagnosed PD (NPD), long-standing PD patients (OPD), and matched healthy controls. Longitudinal sampling in NPD patients—before medication and at multiple points after levodopa initiation—allowed the authors to evaluate early microbial shifts following pharmacologic treatment. The study also integrated clinical indices (UPDRS, Hoehn–Yahr stage, non-motor symptom scores, constipation scores, and mood assessments) to identify correlations between microbial taxa and PD severity.

Who was studied?

Seventy-two Chinese PD patients were enrolled, including 59 with established PD for more than one year (OPD) and 13 newly diagnosed, treatment-naïve individuals (NPD). Sixty-eight healthy spouses or family members served as household-matched controls to minimize dietary and environmental variability. Subjects underwent comprehensive neurological and neuropsychological assessments. Fecal samples were collected from all participants, and longitudinal samples were obtained from the NPD group at baseline and at 3, 5, 7, and 14 days after levodopa initiation. Exclusion criteria included gastrointestinal disease, antibiotic or probiotic use within 90 days, or other unstable medical conditions.

Most important findings

Across pages 2–7, the study presents consistent evidence of gut microbiome disruption in PD. OPD patients showed elevated Rikenellaceae, Porphyromonadaceae, Christensenellaceae, and Clostridiales vadin BB60 group, with reduced Prevotellaceae and Lactobacillaceae. At the genus level, OPD patients exhibited increased Butyricimonas, Parabacteroides, Alistipes, Ruminococcaceae UCG groups, and decreased Prevotella 2 and Prevotella 9. NPD patients displayed significantly elevated Turicibacteraceae and reduced Streptococcus, Ruminococcus, and Paraprevotella before treatment. The plots on pages 3–5 visually show these genus-level contrasts, including the sharp rise in Turicibacter following levodopa initiation.

Clinical correlations (page 6) demonstrated that Eubacterium abundance positively tracked PD severity, while Prevotella and Lachnospira showed negative associations. Microbes linked to short-chain-fatty-acid (SCFA) production—particularly Lachnospiraceae—were depleted in both NPD and OPD patients. LEfSe analysis showed OPD enrichment of Bifidobacterium, Alistipes, Klebsiella, and Tyzzerella, while controls had higher Lactobacillus, Streptococcus, Citrobacter, and Veillonella.

Predictive functional analysis suggested altered microbial metabolic potential: OPD microbiota showed increased pathways related to inflammation, cancer-associated signaling, and branched-chain amino acid biosynthesis, while NPD samples demonstrated shifts in chemotaxis, motility, and xenobiotic degradation pathways.

Key implications

The study reinforces the concept that PD is accompanied by marked gut dysbiosis, with specific taxa—especially reduced Prevotella, Lachnospiraceae, and Lactobacillus and elevated Rikenellaceae, Alistipes, Turicibacter, and Bifidobacterium—emerging as potential microbial signatures. These findings support a mechanistic model linking microbial shifts, SCFA depletion, immune activation, intestinal permeability, and neurodegenerative processes. Medication-associated microbiome changes in NPD patients highlight the bidirectional interaction between host neurobiology and microbial metabolism, emphasizing the importance of microbiome-aware therapeutic strategies.

Citation

Jin M, Li J, Liu F, et al. Analysis of the gut microflora in patients with Parkinson’s disease. Front Neurosci. 2019;13:1184. doi:10.3389/fnins.2019.01184