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

被引：34

作者：

Wood, Paul L. ^{[1
]}

Filiou, Michaela D. ^{[2
]}

Otte, David M. ^{[3
]}

Zimmer, Andreas ^{[3
]}

Turck, Christoph W. ^{[2
]}

机构：

[1] Lincoln Memorial Univ, DeBusk Coll Osteopath Med, Dept Physiol & Pharmacol, Metabol Unit, Harrogate, TN 37752 USA

[2] Max Planck Inst Psychiat, Dept Translat Res Psychiat, D-80804 Munich, Germany

[3] Univ Bonn, Inst Mol Psychiat, D-53127 Bonn, Germany

来源：

SCHIZOPHRENIA RESEARCH | 2014年 / 159卷 / 2-3期

基金：

美国国家卫生研究院;

关键词：

Schizophrenia; Glycosynapse; Sulfatides; Dysconnectivity; Plasmalogens; OXIDATIVE STRESS; OLIGODENDROCYTES; MYELINATION; SULFATIDE; BRAIN;

D O I：

10.1016/j.schres.2014.08.029

中图分类号：

R749 [精神病学];

学科分类号：

100204 [神经病学];

摘要：

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.

引用

页码：365 / 369

页数：5

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