Brain signatures of chronic gut inflammation

Author: Caitlin V Hall1,2,3, Graham Radford-Smith3,4,5, Emma Savage1, Conor Robinson1, Luca Cocchi1,3, Rosalyn J Moran2
1 Clinical Brain Networks Group, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
2 Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, Kings College London, London, United Kingdom.
3 Faculty of Medicine, University of Queensland, Brisbane, QLD, Australia.
4 Gut Health Research Group, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
5 Department of Gastroenterology, Royal Brisbane and Women's Hospital, Brisbane, QLD, Australia.
Conference/Journal: Front Psychiatry
Date published: 2023 Nov 7
Other: Volume ID: 14 , Pages: 1250268 , Special Notes: doi: 10.3389/fpsyt.2023.1250268. , Word Count: 232

Gut inflammation is thought to modify brain activity and behaviour via modulation of the gut-brain axis. However, how relapsing and remitting exposure to peripheral inflammation over the natural history of inflammatory bowel disease (IBD) contributes to altered brain dynamics is poorly understood. Here, we used electroencephalography (EEG) to characterise changes in spontaneous spatiotemporal brain states in Crohn's Disease (CD) (n = 40) and Ulcerative Colitis (UC) (n = 30), compared to healthy individuals (n = 28). We first provide evidence of a significantly perturbed and heterogeneous microbial profile in CD, consistent with previous work showing enduring and long-standing dysbiosis in clinical remission. Results from our brain state assessment show that CD and UC exhibit alterations in the temporal properties of states implicating default-mode network, parietal, and visual regions, reflecting a shift in the predominance from externally to internally-oriented attentional modes. We investigated these dynamics at a finer sub-network resolution, showing a CD-specific and highly selective enhancement of connectivity between the insula and medial prefrontal cortex (mPFC), regions implicated in cognitive-interoceptive appraisal mechanisms. Alongside overall higher anxiety scores in CD, we also provide preliminary support to suggest that the strength of chronic interoceptive hyper-signalling in the brain co-occurs with disease duration. Together, our results demonstrate that a long-standing diagnosis of CD is, in itself, a key factor in determining the risk of developing altered brain network signatures.

Keywords: EEG; IBD; gut-brain; inflammation; microbiome; neuroimaging.

PMID: 38025434 PMCID: PMC10661239 DOI: 10.3389/fpsyt.2023.1250268