ArticleFrontiers in immunology2023
Causality between inflammatory bowel disease and the cerebral cortex: insights from Mendelian randomization and integrated bioinformatics analysis.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Enterococcus hirae Y-HS Alleviates Ulcerative Colitis by Activating PXR/Nrf2-mediated Metabolic-immune Crosstalk.Probiotics and antimicrobial proteins · 2026Article
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- The brain-bone-gut axis: a microbial bridge underlying multisystem comorbidities.Frontiers in endocrinology · 2026Review
- Risk factors for postoperative ileus following transforaminal lumbar interbody fusion: a retrospective study.Journal of orthopaedic surgery and research · 2025Article
- Altered functional connectivity within and between resting-state networks in ulcerative colitis.Brain imaging and behavior · 2025Article
- Diabetes exerts a causal impact on the nervous system within the right hippocampus: substantiated by genetic data.Endocrine · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Background: Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), is a chronic, progressive, and recurrent intestinal condition that poses a significant global health burden. The high prevalence of neuropsychiatric comorbidities in IBD necessitates the development of targeted management strategies. Methods: Leveraging genetic data from genome-wide association studies and Immunochip genotype analyses of nearly 150,000 individuals, we conducted a two-sample Mendelian randomization study to elucidate the driving force of IBD, UC, and CD on cortical reshaping. Genetic variants mediating the causality were collected to disclose the biological pathways linking intestinal inflammation to brain dysfunction. Results: Here, 115, 69, and 98 instrumental variables genetically predicted IBD, UC, and CD. We found that CD significantly decreased the surface area of the temporal pole gyrus (β = -0.946 mm Conclusion: We explore the causality between intestinal inflammation and altered cortical morphology. It is likely that neuroinflammation-induced damage, impaired neurological function, and persistent nociceptive input lead to morphological changes in the cerebral cortex, which may trigger neuropsychiatric disorders.
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Registered trials
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