Gut Microbiota and Metabolome Alterations Associated 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?
The study Gut microbiota and metabolome alterations associated with Parkinson’s disease examined how the Parkinson’s disease gut microbiota and metabolome differ from those of healthy individuals. Using 16S rRNA sequencing and gas chromatography–mass spectrometry, the authors analyzed fecal samples to define microbe–metabolite signatures that connect intestinal dysbiosis to Parkinson’s pathology. This combined profiling allowed researchers to characterize bacterial taxa shifts, evaluate short-chain fatty acid (SCFA)–producing taxa, and map metabolic abnormalities in amino acids, vitamins, lipids, and polyamines. The integration of microbiome and metabolome analyses creates a detailed picture of gut-derived biochemical imbalances linked to neuroinflammation, energy deficits, and perturbations in host–microbe crosstalk relevant to PD pathogenesis.
Who was studied?
The study assessed 64 Italian adults with idiopathic Parkinson’s disease and 51 healthy controls matched primarily through family or spousal relationships. PD participants ranged from Hoehn and Yahr stages I–IV and were receiving stable dopaminergic therapy. Exclusion criteria ensured removal of confounders such as recent antibiotic or probiotic use, active gastrointestinal disease, or major psychiatric or neurological comorbidities. Control subjects reported no constipation and were free of neurological disorders. This well-defined clinical cohort provided a robust framework to analyze gut microbial composition and fecal metabolites across disease and non-disease groups.
Most important findings
PD patients exhibited major depletion of SCFA-producing genera—Lachnospira, Blautia, Butyrivibrio, Roseburia, Coprococcus, and Pseudobutyrivibrio—as clearly visible in the taxonomic heat maps. These taxa, primarily within Lachnospiraceae, are known contributors to gut barrier integrity, anti-inflammatory signaling, and metabolic homeostasis. Concurrent enrichment of Akkermansia, Veillonella, Streptococcus, Escherichia, Enterobacter, Serratia, and Bifidobacterium indicated a community shift toward organisms associated with mucin degradation, lactate accumulation, and increased endotoxin potential. Metabolomics revealed elevated cadaverine, ethanolamine, hydroxypropionic acid, phenylalanine, leucine, isoleucine, and thymine, while linoleic acid, oleic acid, succinic acid, nicotinic acid, pantothenic acid, and pyroglutamic acid were markedly decreased. Correlation matrices showed strong positive associations between Lachnospira-related genera and vitamins B3 and B5, highlighting microbial contributions to micronutrient availability.
Key implications
Findings support the concept that PD involves a gut-based disruption of SCFA production, vitamin biosynthesis, lipid metabolism, and amino acid turnover. Reduced SCFA-producing taxa may impair motility, gut barrier stability, and immune modulation, while diminished B-vitamin–linked pathways suggest compromised microbial nutrient synthesis with implications for mitochondrial energy deficits and oxidative stress. These integrated microbial–metabolite signatures may serve as biomarkers for PD risk stratification, disease progression, or therapeutic targeting.
Citation
Vascellari S, Palmas V, Melis M, Pisanu S, Cusano R, Uva P, et al. Gut microbiota and metabolome alterations associated with Parkinson’s disease.mSystems. 2020;5(5):e00561-20. doi:10.1128/mSystems.00561-20
Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.
Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.
Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.
Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.