Alteration of the fecal microbiota in Chinese patients with Parkinson’s disease Original paper
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Dr. Umar
Read MoreClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
What was studied?
This original research article examined fecal microbiota in Chinese Parkinson’s disease to determine how gut microbial communities differ between patients with Parkinson’s disease (PD) and healthy controls. Using high-throughput Illumina MiSeq sequencing of the 16S rRNA V3–V4 region, the investigators analyzed fecal samples from matched couples—each PD patient and their cohabiting spouse—to tightly control for shared environmental and dietary influences. The study specifically assessed microbial diversity, taxonomic composition, functional gene predictions, and correlations between bacterial genera and clinical measures of PD, including disease duration, motor severity, medication exposure, and non-motor symptoms. Sequencing generated more than 9 million reads, allowing robust comparisons of microbial richness and structure. By focusing on genus-level differences, the study aimed to clarify microbial signatures potentially contributing to PD pathogenesis and identify taxa relevant to microbiome-based diagnostic or therapeutic strategies.
Who was studied?
The study enrolled 45 individuals diagnosed with idiopathic PD and their 45 healthy spouses as matched controls, all living in the same household in Shanghai. Patients met UK Brain Bank diagnostic criteria and had no major chronic illnesses that could confound microbiome composition. Spouses were screened to exclude gastrointestinal conditions, particularly irritable bowel syndrome, and neither group had taken antibiotics or probiotic supplements within three months of fecal sampling. PD participants had a mean age of about 68 years, an average disease duration of ~6 years, and were all receiving antiparkinsonian medications, with levodopa equivalent doses recorded to explore microbiota–drug interactions. Clinical assessments included motor severity (UPDRS scores, Hoehn & Yahr stage), constipation, depression and anxiety scales, and cognitive evaluations using MMSE and MoCA. This well-controlled sampling design minimized dietary variability and facilitated cleaner attribution of microbiome differences to disease status rather than environmental factors.
Most important findings
PD patients exhibited significantly higher alpha-diversity across multiple metrics and distinct beta-diversity patterns, indicating altered gut microbial structure. Several genera—including Clostridium IV, Clostridium XVIII, Butyricicoccus, Holdemania, Sphingomonas, Anaerotruncus, and Aquabacterium—were enriched in PD after adjusting for age, sex, BMI, and constipation. In contrast, Lactobacillus was more abundant in healthy spouses. Functional gene predictions showed reduced pathways involving vitamin and cofactor metabolism in PD, alongside increased microbial genes associated with energy metabolism and fatty acid biosynthesis. Clinically meaningful correlations included negative associations between Escherichia/Shigella and disease duration, and inverse relationships of Dorea and Phascolarctobacterium with levodopa equivalent dose. Butyricicoccus and Clostridium XIVb were linked with worse cognitive performance, indicating microbiome involvement in non-motor manifestations.
Key implications
These findings reinforce the concept that PD involves systemic, gut-linked pathophysiology characterized by taxonomic shifts, functional reprogramming of microbial gene pathways, and disease-relevant microbial associations. Dysbiosis included enrichment of genera implicated in inflammation, mucosal barrier disruption, and altered short-chain fatty acid metabolism—microbial activities suspected to influence α-synuclein aggregation and neuroinflammation. The demonstrated associations with clinical severity, medication exposure, and cognitive impairment strengthen the hypothesis that gut microbes influence PD progression and symptom expression. Such results support ongoing efforts to develop microbiome-informed biomarkers and targeted microbial therapies, particularly during prodromal stages when disease-modifying interventions may be most effective.
Citation
Qian Y, Yang X, Xu S, et al. Alteration of the fecal microbiota in Chinese patients with Parkinson’s disease. Brain Behavior and Immunity. 2018. doi:10.1016/j.bbi.2018.02.016