ArticleScientific reports2025
Causal effects of brain subregion gene expression on inflammatory bowel diseases revealed by Mendelian randomization and single cell analysis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Advances in Oral Cavity Stem Cell Research Revealed through Multi-omics Analysis.Stem cell reviews and reports · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Inflammatory Bowel Diseases (IBDs), including Ulcerative Colitis (UC) and Crohn's Disease (CD), are chronic gastrointestinal disorders. The gut-brain axis integrates various signals, but its impact on IBD is unclear. Using Mendelian Randomization, we evaluated causal relationships between 13 brain subregions and colon expression quantitative trait loci (eQTLs) with IBDs. Trans-omics analysis, integrating brain, CD and UC intestine single-cell RNA sequencing and genomic eQTLs, identified cellular sources of key genes. Phenome-Wide Association Studies (PheWAS) filtered phenotype associations of leading SNPs. Brain eQTLs showed meaningful associations with IBD susceptibility, with consistent patterns observed across multiple independent cohorts (IIBDGC, UKB, and FinnGen). However, correlation analysis revealed that eQTL sample sizes significantly influence the detection of significant associations (r = 0.53-0.90), indicating that direct quantitative comparisons between tissues should be interpreted cautiously. Multiple brain regions, including the cerebellum, cerebellar hemisphere, and cortex, demonstrated notable associations with IBD. Exploratory analysis identified genes CCDC88B, NAAA and NAGLU showing putative positive causal associations with IBD susceptibility in both brain and colon tissues, whereas CWC15 exhibited an inverse relationship. Stringent Bonferroni correction validated CCDC88B and NAGLU as robust candidates across multiple tissues and IBD subtypes. Single-cell RNA sequencing identified dendritic cells and epithelial cells as sources of NAAA and CWC15, respectively, enriched in inflammatory pathways. PheWAS showed leading SNPs associated with metabolic dysfunction, immune disorders, and brain imaging measures. This study demonstrates meaningful brain-gut axis involvement in IBD pathogenesis while acknowledging methodological limitations in cross-tissue comparisons. The identified candidate genes and cellular mechanisms provide new insights for understanding IBD susceptibility and potential therapeutic targets.
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Registered trials
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