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Journal Article

Lipidomics reveals dysfunctional glycosynapses in schizophrenia and the G72/G30 transgenic mouse

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Filiou,  Michaela D.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Turck,  Christoph W.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Wood, P. L., Filiou, M. D., Otte, D. M., Zimmer, A., & Turck, C. W. (2014). Lipidomics reveals dysfunctional glycosynapses in schizophrenia and the G72/G30 transgenic mouse. SCHIZOPHRENIA RESEARCH, 159(2-3), 365-369. doi:10.1016/j.schres.2014.08.029.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0026-CEC9-B
Abstract
Background: Abnormal structural/functional connectivity has been proposed to underlie the pathophysiology of schizophrenia. However, the biochemical basis of abnormal connectivity remains undefined. Methods: We undertook a shotgun lipidomic analysis of over 700 lipids across 26 lipid subclasses in the frontal cortex of schizophrenia subjects and hippocampus of G72/G30 transgenic mice. Results: We demonstrate that glycosphingolipids and choline plasmalogens, structural lipid pools in myelin, are significantly elevated in the frontal cortex obtained from patients suffering from schizophrenia and the hippocampus of G72/G30 transgenic mice. Conclusions: Our data suggest that structural lipid alterations in oligodendrocyte glycosynapses are responsible for dysconnectivity in schizophrenia and that increased expression of G72 protein may play a role in the development of abnormal glycosynapses. (C) 2014 Elsevier B. V. All rights reserved.