ArticleNPJ Parkinson's disease2025
Strain-specific effects of Desulfovibrio on neurodegeneration and oxidative stress in a Caenorhabditis elegans PD model.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Article
- From dysbiosis to dysfunction: specific gut microbes and metabolites in the pathogenesis of Parkinson's disease.Sustainable microbiology · 2026Review
- Inulin ameliorates chronic ketamine-induced anxiety-like behaviors and impairments in spatial learning and memory: involvement of gut microbiota, microbial metabolite short-chain fatty acids, and the BDNF-TrkB-ERK1/2-CREB pathway.Frontiers in microbiology · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The gut microbiota is increasingly recognized as a key contributor to intestinal and brain pathologies, including Parkinson's disease (PD). Sulfate-reducing Desulfovibrio (DSV) species have emerged as microbial drivers through hydrogen sulfide and other neurotoxic factors. Using the Caenorhabditis elegans PD model NL5901 expressing human α-synuclein, we examined the effects of six DSV strains from human, animal, and environmental sources on food preference, α-syn aggregation, ROS production, gene expression, and lifespan. C. elegans strongly preferred environmental strains, particularly D. vulgaris DSM 644 (94.7% vs. 5.3% over D. piger DSM 749). In contrast, the animal isolate D. desulfuricans DSM 6949 and PD isolate D. spp. MUU 26 induced the highest α-syn aggregation (49.05 and 40.15 aggregates), ROS (3.42-fold, 3.01-fold), and sod-3, daf-16, and hsp-16.1 repression. DSM 644-fed worms exhibited a protective transcriptional profile and the greatest lifespan extension (median 36 days). These results highlight strain-specific effects of DSV on neurodegeneration, oxidative stress, and aging, reinforcing the need for mechanistic validation in mammalian PD models.
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Registered trials
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