The link between increased Desulfovibrio and disease severity in Parkinson’s disease Original paper
Researched by:
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Dr. Umar
ID
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.
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Dr. Umar
Read More
Researched by:
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Dr. Umar
ID
Dr. Umar
Read More
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
Location
China
Sample Site
Feces
Species
Homo sapiens
What was studied?
This original study investigated Desulfovibrio and Parkinson’s disease using a combined 16S rRNA amplicon and shotgun metagenomic approach to link gut microbiome features with clinical disease severity. The authors enrolled newly diagnosed, untreated Parkinson’s disease (PD) patients and matched healthy controls, then profiled their fecal microbiota to identify taxa and microbial functions associated not just with PD status but with Hoehn and Yahr stage. They focused on ecological assembly processes (e.g., homogeneous selection vs drift) to understand why specific taxa expand in PD. Metagenome-assembled genomes (MAGs) were reconstructed to pinpoint Desulfovibrio strains—especially one genome, MAG58—with detailed sulfur metabolism capacity, enabling mechanistic hypotheses around hydrogen sulfide–mediated neurotoxicity and PD progression.
Who was studied?
The cohort comprised 47 newly diagnosed, drug-naïve PD patients and 43 age- and sex-matched healthy controls, all recruited from Peking University Third Hospital in China. PD diagnosis followed the International Parkinson’s Disease and Movement Disorder Society criteria. Clinical phenotyping included Hoehn and Yahr staging, MDS-UPDRS, cognitive and mood scales, enabling stratification of PD subjects by motor severity (stages 1.0–2.5). Stool samples were collected before any dopaminergic or other chronic PD medication, reducing confounding by treatment-related microbiome shifts that complicate many previous PD microbiome datasets.
Most important findings
Gut community structure differed between PD and controls, but the standout signal was a significant increase in Desulfovibrio abundance in PD, with Desulfovibrio levels positively correlated with PD severity across Hoehn and Yahr stages. Community assembly analysis suggested this Desulfovibrio enrichment was driven by enhanced homogeneous selection (strong, consistent environmental filtering) and weakened ecological drift, indicating an active selective advantage rather than random fluctuation.
Metagenomic reconstruction yielded multiple MAGs, including Desulfovibrio MAG58, whose relative abundance also tracked with PD severity. MAG58 encoded a complete assimilatory sulfate reduction pathway and a near-complete dissimilatory sulfate reduction pathway, supporting robust hydrogen sulfide (H₂S) production capacity. This aligns with broader literature implicating sulfate-reducing Desulfovibrio species and their H₂S output in neurodegenerative mechanisms and α-synuclein aggregation.
Using four severity-associated amplicon sequence variants (ASVs), including Desulfovibrio-related taxa, the authors could predict PD severity with about 77% accuracy via random forest modeling, suggesting potential microbiome-based biomarkers for staging.
Key implications
Clinically, this work supports Desulfovibrio as a candidate pathobiont and progression marker in PD rather than a mere diagnostic discriminator. The combination of severity-associated abundance, non-random ecological expansion, and explicit H₂S-production pathways in MAG58 underpins a mechanistic model: excess bacterial H₂S in the gut may damage epithelial and neural interfaces, promote systemic inflammation, and facilitate α-synuclein misfolding and propagation along the gut–brain axis. For clinicians, Desulfovibrio-enriched signatures could evolve into stool-based tools for risk stratification or monitoring, while therapeutically, targeting sulfate-reducing bacteria (diet, probiotics, phage, or selective antibiotics) becomes a tangible intervention hypothesis to slow PD progression—though interventional data are not yet available and will be crucial before translation into practice.
Citation
Nie S, Jing Z, Wang J, et al. The link between increased Desulfovibrio and disease severity in Parkinson’s disease. Applied Microbiology and Biotechnology. 2023;107(9):3033-3045. doi:10.1007/s00253-023-12489-1