학술논문

Functional brain rewiring and altered cortical stability in ulcerative colitis
Document Type
article
Source
Molecular Psychiatry. 27(3)
Subject
Behavioral and Social Science
Digestive Diseases
Inflammatory Bowel Disease
Clinical Research
Neurosciences
Mental Health
Basic Behavioral and Social Science
Autoimmune Disease
2.1 Biological and endogenous factors
Underpinning research
1.1 Normal biological development and functioning
Aetiology
Neurological
Mental health
Oral and gastrointestinal
Brain
Colitis
Ulcerative
Connectome
Humans
Inflammation
Irritable Bowel Syndrome
Biological Sciences
Medical and Health Sciences
Psychology and Cognitive Sciences
Psychiatry
Language
Abstract
Despite recent advances, there is still a major need to better understand the interactions between brain function and chronic gut inflammation and its clinical implications. Alterations in executive function have previously been identified in several chronic inflammatory conditions, including inflammatory bowel diseases. Inflammation-associated brain alterations can be captured by connectome analysis. Here, we used the resting-state fMRI data from 222 participants comprising three groups (ulcerative colitis (UC), irritable bowel syndrome (IBS), and healthy controls (HC), N = 74 each) to investigate the alterations in functional brain wiring and cortical stability in UC compared to the two control groups and identify possible correlations of these alterations with clinical parameters. Globally, UC participants showed increased functional connectivity and decreased modularity compared to IBS and HC groups. Regionally, UC showed decreased eigenvector centrality in the executive control network (UC  IBS > HC). UC also showed increased connectivity in dorsal attention, somatomotor network, and visual networks, and these enhanced subnetwork connectivities were able to distinguish UC participants from HCs and IBS with high accuracy. Dynamic functional connectome analysis revealed that UC showed enhanced cortical stability in the medial prefrontal cortex (mPFC), which correlated with severe depression and anxiety-related measures. None of the observed brain changes were correlated with disease duration. Together, these findings are consistent with compromised functioning of networks involved in executive function and sensory integration in UC.