Altered gut microbiota and inflammatory cytokine responses in patients with Parkinson’s disease Original paper
-
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?
Altered gut microbiota in Parkinson’s disease was investigated to clarify how taxonomic shifts and inflammatory cytokine responses might contribute to neurodegeneration. The study sequenced V3–V4 16S rRNA regions from fecal samples and measured plasma cytokines, examining whether microbial signatures correlated with clinical motor severity and systemic inflammation. Findings were validated in an independent cohort to strengthen reliability.
Who was studied?
The research analyzed 80 Taiwanese patients with Parkinson’s disease and 77 age- and sex-matched controls, all carefully screened to exclude gastrointestinal disease, recent antibiotic/probiotic use, and major confounders. An additional cohort of 120 PD patients and 120 controls was used to confirm cytokine alterations. Clinical characterization included UPDRS III scoring, motor subtype classification, constipation assessment, and dietary analysis.
Most important findings
Patients exhibited markedly altered gut microbial composition, with increased Verrucomicrobia, Mucispirillum, Porphyromonas, Lactobacillus, and Parabacteroides, while Prevotella was substantially reduced (page 1 summary; page 4 LDA chart). Prevotella abundance was 46.6% lower in PD, reinforcing its protective role in mucin production and gut barrier integrity. Bacteroides was elevated in the non-tremor subtype and strongly correlated with UPDRS III motor severity (rho ≈ 0.64). Diverse β-diversity profiles (page 4 PCoA plots) showed clear separation between PD and control microbiomes. Elevated cytokines—particularly TNFα and IFNγ—were linked to specific microbes: Bacteroides correlated with TNFα, while Verrucomicrobia correlated with IFNγ. These cytokine elevations were replicated in the second cohort, indicating systemic inflammatory activation associated with dysbiosis.
Key implications
The study demonstrates that altered gut microbiota in Parkinson’s disease may influence immune activation, contributing to neuroinflammation and potentially accelerating symptom progression. Reduced Prevotella suggests impaired mucous barrier function and increased gut permeability, while elevated Bacteroides highlights microbe-driven inflammatory cytokine signaling that may exacerbate motor decline. These microbial signatures may form the basis for diagnostic biomarkers or therapeutic targets aimed at modifying gut-immune interactions in PD.
Citation
Lin C-H, Chen C-C, Chiang H-L, et al. Altered gut microbiota and inflammatory cytokine responses in patients with Parkinson’s disease. Journal of Neuroinflammation. 2019;16(129). doi:10.1186/s12974-019-1528-y