ArticleMedicine2026
Bidirectional mediation between microbiota and immune system in Parkinson disease: A two-sample Mendelian randomization study.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Gut-Brain-Skin Axis: From Mechanistic Insights to Translational Applications in Neurocosmetics.Dermatology and therapy · 2026Review
- Causal Effects of Circulating Inflammatory Proteins on Postmenopausal Atrophic Vaginitis in European Populations: A Mendelian Randomization Study with Transcriptomic Validation.International journal of women's health · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies suggest that gut and skin microbiota, immune cells, and inflammatory proteins may contribute to the development of Parkinson disease (PD). However, their causal relationships and underlying mediating mechanisms remain unclear. We conducted a two-sample Mendelian randomization analysis using publicly available genome-wide association study summary data to evaluate the causal relationships among 473 gut and 150 skin microbiota, 731 immune cell phenotypes, 91 inflammatory proteins, and PD. Sensitivity analyses and mediation analyses were conducted to evaluate robustness and explore potential biological pathways. We identified 16 gut microbial taxa, 2 skin microbiota, 19 immune cell phenotypes, and 4 inflammatory proteins with significant causal associations with PD. Two-step mediation Mendelian randomization further revealed multiple potential pathways of "microbiota-immune-PD" and "immune-microbiota-PD." For instance, HLA DR on myeloid dendritic cells mediated 14.80% of the effect of Gammaproteobacteria_Sebaceous on PD risk, while Species Bifidobacterium adolescentis mediated 10.50% the protective effect of CD28- CD8dim %T cell. Notably, IL-18 exhibited the highest mediation proportion (26.4%) via the family Lentimicrobiaceae. Our findings provide novel genetic evidence supporting the role of the microbiota-immune axis in PD pathogenesis and highlight potential targets for therapeutic intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.