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\begin{document}

\title{Brain network topological changes in inflammatory bowel disease: an
exploratory study}



\author[1]{Arianna Polverino}%
\author[2]{Emahnuel  Troisi Lopez}%
\author[3]{Roberta Minino}%
\author[3]{Antonella Romano}%
\author[4]{Agnese Miranda}%
\author[5]{Angela Facchiano}%
\author[3]{Lorenzo Cipriano}%
\author[2]{Pierpaolo Sorrentino}%
\affil[1]{Institute of Diagnosis and Treatment Hermitage Capodimonte}%
\affil[2]{National Research Council}%
\affil[3]{University of Naples Parthenope}%
\affil[4]{University of Campania Luigi Vanvitelli}%
\affil[5]{Umberto I General Hospital}%


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  \date{May 21, 2024}


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\begin{abstract}
Although the etio-pathogenesis of inflammatory bowel diseases (IBD) is
not entirely clear, the interaction between genetic and adverse
environmental factors may reduce the variety of the intestinal
microbiota (dysbiosis), resulting in a chronic inflammation having
effects on the large-scale brain network through the gut-brain axis. In
this paper, we hypothesized the presence of inflammation-related changes
in brain topology of IBD patients, regardless of the specific clinical
form (ulcerative colitis (UC) or Crohn's disease (CD)). To test this
hypothesis, we analyzed source-reconstructed magnetoencephalography
(MEG) signals in 25 IBD patients and 28 healthy controls (HC) in
resting-state condition, and evaluated the brain network topology.
Finally, to assess whether these changes were linked to IBD clinical
evolution, we correlated brain topology to disease duration. We found
that the betweenness centrality (BC) of the left hippocampus was higher
in patients as compared to controls, in the gamma frequency band. BC is
a nodal topological parameter indicating how much a brain region is
involved in the flow of information through the brain network.
Furthermore, the comparison among UC, CD and HC showed statistically
significant differences between UC and HC and between CD and HC, but not
between the two clinical forms. Our results demonstrated that the
topological changes observed in IBD patients were not dependent on the
specific clinical form, but due to the gastro-intestinal inflammatory
process itself. However, although these findings are promising, we need
to enlarge the sample size to monitor the brain involvement in IBD and
to clarify the clinical impact.%
\end{abstract}%



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