Gut microbiota in Parkinson disease in a northern German cohort Original paper

What was studied?

This study investigated Parkinson’s disease gut microbiota composition in a northern German cohort to determine whether individuals with Parkinson’s disease (PD) exhibit distinct microbial signatures compared with age-matched controls. Using next-generation sequencing of the bacterial 16S rRNA gene from stool samples, the researchers examined whether PD is associated with meaningful qualitative or quantitative alterations in gut microbial communities. The analysis included assessments of alpha diversity, beta diversity, and family-level taxonomic abundances. Because emerging evidence suggests that PD may originate in the enteric nervous system and progress toward the central nervous system via vagal pathways, the study aimed to clarify whether PD-associated dysbiosis could support this pathogenic framework.

Who was studied?

Fifty-eight adults were included, consisting of 29 PD cases and 29 age-matched controls recruited at Kiel University’s Department of Neurology. Mean age was nearly identical between groups (about 69 years), but sex distribution differed, with PD cases predominantly male. All participants were omnivores without recent antibiotic exposure or gastrointestinal disease. PD diagnoses were confirmed by movement-disorder specialists using established clinical criteria, and non-motor symptoms such as constipation were more common in PD patients, consistent with known prodromal features. Stool samples were collected either in the hospital or shortly after discharge and processed under consistent laboratory conditions. Controls were clinically evaluated to exclude prodromal PD features such as hyposmia, REM-sleep behavior disorder, constipation, or depression.

Most important findings

The investigators found no differences in alpha diversity (richness and evenness metrics such as Shannon, Simpson, Chao1) or in major bacterial phyla. However, unweighted UniFrac analysis revealed significant beta-diversity separation, indicating distinct community composition between PD and control groups.

Family-level assessments identified three families elevated in PD after adjustment for sex, diet-related factors, nicotine use, caffeine intake, constipation, alcohol use, cardiovascular comorbidity, and sequencing batch:

The ROC analysis combining these three microbial families achieved an AUC of 0.83, suggesting potential for microbial biomarkers, though likely overestimated due to discovery-stage sampling. Page-3 visualizations confirm marked dispersion patterns, with higher counts of these taxa clustering in PD groups.

Key implications

The findings strengthen the evidence that PD is associated with distinct gut microbiota signatures, particularly elevated Lactobacillaceae, Barnesiellaceae, and Enterococcaceae. These microbial shifts may influence intestinal permeability, neuroimmune activation, or short-chain fatty acid dynamics, all of which could affect enteric–central nervous system communication. However, the modest sample size, sex imbalance, and potential medication effects limit direct clinical translation. Future large, well-controlled multicenter studies—including drug-naïve patients—are essential to validate microbial biomarkers and clarify whether gut dysbiosis contributes to PD pathogenesis or arises secondary to disease-related physiology or pharmacologic treatment.

Citation

Hopfner F, Künstner A, Müller SH, et al. Gut microbiota in Parkinson’s disease in a northern German cohort. Brain Res. 2017;1667:41-45