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. 2020 Sep 14;31(1):448–462. doi: 10.1093/cercor/bhaa236

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© The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Potential mechanism of corpus callosum abnormality development in schizophrenia. In schizophrenia, reduced and dysfunctional microglial cells result in abnormal cross-talk with oligodendrocytes via mediators such as IL1B and TGFB1. This leads to transcriptional perturbation caused by impaired schizophrenia-related gene network including NFATC2 and CSF1R, resulting in abnormal lipid metabolism. This disturbs the normal properties and functions of oligodendrocytes and the myelin sheath, causing structural and functional deficits in the corpus callosum.