Lipidomics reveals dysfunctional glycosynapses in schizophrenia and the G72/G30 transgenic mouse
Lipidomics reveals dysfunctional glycosynapses in schizophrenia and the G72/G30 transgenic mouse
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DOI：
10.1016/j.schres.2014.08.029
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发表时间：
2014-11-01
影响因子：
4.5
通讯作者：
Turck, Christoph W.
中科院分区：
文献类型：
--
作者：
Wood, Paul L.;Filiou, Michaela D.;Turck, Christoph W.
背景：结构/功能连接异常被认为是精神分裂症病理生理学的基础。然而，异常连接的生化基础仍然undefined.Methods：我们进行了鸟枪脂质组学分析超过700脂质横跨26脂质亚类在额叶皮质的精神分裂症受试者和海马G72/G30转基因小鼠。我们证明了鞘糖脂和胆碱缩醛磷脂，髓鞘中的结构脂质池，在精神分裂症患者的额叶皮层和G72/G30转基因小鼠的海马中显著升高。我们的数据表明，少突胶质细胞糖突触中结构脂质的改变是精神分裂症连接障碍的原因，G72表达的增加蛋白质可能在异常糖突触的发展中起作用。(C)2014年爱思唯尔B。V.保留所有权利。
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.