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蛋白质组和转录组分析表明精神分裂症中少突胶质细胞功能障碍。

Proteome and transcriptome analysis suggests oligodendrocyte dysfunction in schizophrenia.

机构信息

Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, D-80804 Munich, Germany.

出版信息

J Psychiatr Res. 2010 Feb;44(3):149-56. doi: 10.1016/j.jpsychires.2009.07.007. Epub 2009 Aug 21.

Abstract

Despite all the efforts regarding the treatment of schizophrenia patients and the growing advances in molecular diagnosis studies, the biochemical basis of this debilitating psychotic mental disorder that affects approximately 1% of the world's population is still not completely comprehended. Several recent clinical and molecular studies, using transcriptome and proteome analyses (TPA), for example, have described the oligodendrocyte dysfunction as a significant feature of the disease. TPA has been extensively used as a biomarker discovery tool, but a detailed and careful interpretation of the generated data can also provide a picture of the integrated biochemical systems that lead to the disease. This review presents the oligodendrocyte role players in schizophrenia pathogenesis as revealed by transcriptome and proteome studies. The presented data contribute to the composition of a scenario that may lead to a better understanding of schizophrenia pathogenesis.

摘要

尽管在精神分裂症患者的治疗方面已经做出了种种努力,并且分子诊断研究也取得了不断的进展,但这种影响全球约 1%人口的使人虚弱的精神疾病的生物化学基础仍未被完全理解。最近的几项临床和分子研究,例如使用转录组和蛋白质组分析(TPA),已经描述了少突胶质细胞功能障碍是该疾病的一个重要特征。TPA 已被广泛用作生物标志物发现工具,但对生成数据的详细和仔细解释也可以提供导致疾病的综合生化系统的图片。这篇综述介绍了转录组和蛋白质组研究揭示的少突胶质细胞在精神分裂症发病机制中的作用。所呈现的数据有助于构建一种可能有助于更好地理解精神分裂症发病机制的情景。

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