Multiomics analysis of the gut-microbiota-brain axis shows neural signatures of Crohn’s disease and its underlying mechanisms
Motivation: Neural alterations affect intestinal conditions. However, these neural alterations and their potential formation mechanisms remain unclear. Goal(s): We integrated brain radiomics, the fecal microbiome, and blood metabolomics to investigate neural characteristics in patients with Crohn’s disease (CD) by establishing putative links between the gut microbiota, blood metabolites, and brain alterations. Approach: Multiomics data were compared between CD patients and healthy controls. Results: We developed a novel multiparameter brain MRI-based radiomics model to characterize the neural features of CD patients. Causal mediation analysis revealed significant pathways supporting the pivotal role of the gut-brain axis in neural alterations in CD patients. Impact: We developed a novel multiparameter MRI-based radiomics model to comprehensively characterize neural alterations in patients with Crohn’s disease. We presented biologically plausible evidence of the formation mechanism underlying these alterations from a gut-microbiota-brain axis perspective.
Authors
- Xiaodi Shen (ORCID: https://orcid.org/0000-0002-4754-8415)
- Ren Mao (ORCID: https://orcid.org/0000-0002-5523-8185)
- Shi‐Ting Feng (ORCID: https://orcid.org/0000-0002-0869-7290)
- Mengzhu Wang (ORCID: https://orcid.org/0000-0002-1059-0441)
- R Zhang (ORCID: https://orcid.org/0000-0002-2815-4584)
- Y. Wang
- Zhao Chen (ORCID: https://orcid.org/0000-0002-6840-316X)
- Xuehua Li (ORCID: https://orcid.org/0000-0002-7476-2644)
- Li Huang
Publication Details
- Journal
- Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition
- Published
- 2024-11-26
- DOI
- https://doi.org/10.58530/2024/0743
- Primary Topic
- Gut microbiota and health
- Type
- article
- Field-Weighted Citation Impact
- 0.00