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June 1, 2026Frontiers in Cellular and Infection Microbiology0 citationsOpen Access

Specific gut microbiota alterations and metabolic deficits in Parkinson’s disease: a controlled comparison with functional constipation

SYShuang YangCTChen TianDPDing Peng

Key Points

  • This study aims to identify Parkinson’s disease-specific gut microbiota differences that are not related to motility changes from constipation.
  • Compared fecal microbiota of Parkinson’s disease patients with constipation (n=20) to functional constipation controls (n=15).
  • Employed high-throughput 16S rRNA gene sequencing and functional prediction of fecal samples.
  • Analyzed diversity metrics and taxonomic compositions to detect Parkinson’s disease-specific signatures.
  • The PDC group had higher microbial richness compared to the FC group (P=0.01).
  • Identified compositional shifts in PDC, including higher levels of Paraprevotella, Akkermansia, unclassified Ruminococcaceae, and Campylobacter.
  • Significant deficits in tyrosine and glutathione metabolic pathways were observed in the PDC group (P<0.05).

Abstract

Objective To isolate Parkinson’s disease (PD)-specific gut dysbiosis from motility-related changes, this study compared the fecal microbiota of PD patients with constipation (PDC, n=20) against a functional constipation (FC, n=15) control group. Methods High-throughput 16S rRNA gene sequencing and functional prediction were performed on fecal samples. Diversity metrics and taxonomic compositions were analyzed to identify PD-specific signatures. Results The PDC group exhibited significantly higher microbial richness than the FC group (P = 0.01). Despite structural similarities driven by the shared constipation phenotype (ANOSIM R = 0.084), PDC was distinguished by specific compositional shifts, including the enrichment of Paraprevotella , Akkermansia , unclassified Ruminococcaceae , and Campylobacter . Functionally, the PDC microbiome showed significant deficits in tyrosine and glutathione metabolism pathways (P0.05), indicating compromised dopamine precursor synthesis and antioxidant defense. Conclusion By controlling for colonic transit time, this study identified specific microbial alterations and metabolic deficits in PD independent of constipation. These findings support a “gut-first” etiology linked to specific pathobionts and barrier compromise.

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Cite This Study

Yang et al. (2026) studied this question.

synapsesocial.com/papers/6a1d20f302fbce9130637398https://doi.org/10.3389/fcimb.2026.1767241
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