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Intrinsic neural network dysfunction in quiescent Crohn’s Disease

Psychological factors and comorbidities play an important role in inflammatory bowel diseases. Such comorbidity could be associated with a specific neural phenotype. Brain regions associated with emotion regulation and self-referential processing, including areas assigned to the “default mode networ...

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Autores principales: Thomann, Anne K., Griebe, Martin, Thomann, Philipp A., Hirjak, Dusan, Ebert, Matthias P., Szabo, Kristina, Reindl, Wolfgang, Wolf, Robert C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599642/
https://www.ncbi.nlm.nih.gov/pubmed/28912568
http://dx.doi.org/10.1038/s41598-017-11792-y
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author Thomann, Anne K.
Griebe, Martin
Thomann, Philipp A.
Hirjak, Dusan
Ebert, Matthias P.
Szabo, Kristina
Reindl, Wolfgang
Wolf, Robert C.
author_facet Thomann, Anne K.
Griebe, Martin
Thomann, Philipp A.
Hirjak, Dusan
Ebert, Matthias P.
Szabo, Kristina
Reindl, Wolfgang
Wolf, Robert C.
author_sort Thomann, Anne K.
collection PubMed
description Psychological factors and comorbidities play an important role in inflammatory bowel diseases. Such comorbidity could be associated with a specific neural phenotype. Brain regions associated with emotion regulation and self-referential processing, including areas assigned to the “default mode network” (DMN), could be promising candidates in this regard. We investigated the functional integrity of multiple intrinsic neural networks in remitted patients with Crohn’s disease (CD) and sought to establish relationships between neural network connectivity and psychiatric symptoms. Fifteen CD patients in remission and 14 controls were investigated. We employed resting-state functional magnetic resonance imaging (fMRI) at 3 Tesla followed by a spatial Independent Component Analysis for fMRI data. Abnormal connectivity in CD patients was observed in DMN subsystems only (p < 0.05, cluster-corrected). Increased connectivity was found in the anterior cingulate and left superior medial frontal gyrus (aDMN) and the middle cingulate cortex (pDMN). Middle cingulate activity showed a significant association with anxiety scores in patients (p = 0.029). This study provides first evidence of selectively disrupted intrinsic neural network connectivity in CD and suggests abnormalities of self-referential neural networks. An increased sensitivity to self-related affective and somatic states in CD patients could account for these findings and explain a higher risk for anxiety symptoms.
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spelling pubmed-55996422017-09-15 Intrinsic neural network dysfunction in quiescent Crohn’s Disease Thomann, Anne K. Griebe, Martin Thomann, Philipp A. Hirjak, Dusan Ebert, Matthias P. Szabo, Kristina Reindl, Wolfgang Wolf, Robert C. Sci Rep Article Psychological factors and comorbidities play an important role in inflammatory bowel diseases. Such comorbidity could be associated with a specific neural phenotype. Brain regions associated with emotion regulation and self-referential processing, including areas assigned to the “default mode network” (DMN), could be promising candidates in this regard. We investigated the functional integrity of multiple intrinsic neural networks in remitted patients with Crohn’s disease (CD) and sought to establish relationships between neural network connectivity and psychiatric symptoms. Fifteen CD patients in remission and 14 controls were investigated. We employed resting-state functional magnetic resonance imaging (fMRI) at 3 Tesla followed by a spatial Independent Component Analysis for fMRI data. Abnormal connectivity in CD patients was observed in DMN subsystems only (p < 0.05, cluster-corrected). Increased connectivity was found in the anterior cingulate and left superior medial frontal gyrus (aDMN) and the middle cingulate cortex (pDMN). Middle cingulate activity showed a significant association with anxiety scores in patients (p = 0.029). This study provides first evidence of selectively disrupted intrinsic neural network connectivity in CD and suggests abnormalities of self-referential neural networks. An increased sensitivity to self-related affective and somatic states in CD patients could account for these findings and explain a higher risk for anxiety symptoms. Nature Publishing Group UK 2017-09-14 /pmc/articles/PMC5599642/ /pubmed/28912568 http://dx.doi.org/10.1038/s41598-017-11792-y Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Thomann, Anne K.
Griebe, Martin
Thomann, Philipp A.
Hirjak, Dusan
Ebert, Matthias P.
Szabo, Kristina
Reindl, Wolfgang
Wolf, Robert C.
Intrinsic neural network dysfunction in quiescent Crohn’s Disease
title Intrinsic neural network dysfunction in quiescent Crohn’s Disease
title_full Intrinsic neural network dysfunction in quiescent Crohn’s Disease
title_fullStr Intrinsic neural network dysfunction in quiescent Crohn’s Disease
title_full_unstemmed Intrinsic neural network dysfunction in quiescent Crohn’s Disease
title_short Intrinsic neural network dysfunction in quiescent Crohn’s Disease
title_sort intrinsic neural network dysfunction in quiescent crohn’s disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599642/
https://www.ncbi.nlm.nih.gov/pubmed/28912568
http://dx.doi.org/10.1038/s41598-017-11792-y
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