脂质组学揭示精神分裂症及G72/G30转基因小鼠中功能失调的糖突触。
Lipidomics reveals dysfunctional glycosynapses in schizophrenia and the G72/G30 transgenic mouse.
作者信息
Wood Paul L, Filiou Michaela D, Otte David M, Zimmer Andreas, Turck Christoph W
机构信息
Metabolomics Unit, Department of Physiology and Pharmacology, DeBusk College of Osteopathic Medicine, Lincoln Memorial University, 6965 Cumberland Gap Pkwy., Harrogate, TN 37752, USA.
Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Kraepelinstr. 2-10, Munich D-80804, Germany.
出版信息
Schizophr Res. 2014 Nov;159(2-3):365-9. doi: 10.1016/j.schres.2014.08.029. Epub 2014 Sep 26.
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.
背景
异常的结构/功能连接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不明确。
方法
我们对精神分裂症患者额叶皮质和G72/G30转基因小鼠海马体中26个脂质亚类的700多种脂质进行了鸟枪法脂质组学分析。
结果
我们证明，糖鞘脂和胆碱缩醛磷脂（髓鞘中的结构脂质库）在精神分裂症患者的额叶皮质和G72/G30转基因小鼠的海马体中显著升高。
结论
我们的数据表明，少突胶质细胞糖突触中的结构脂质改变是精神分裂症中连接障碍的原因，并且G72蛋白表达增加可能在异常糖突触的发展中起作用。
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