Advancements in the Underlying Pathogenesis of Schizophrenia: Implications of DNA Methylation in Glial Cells.
Advancements in the Underlying Pathogenesis of Schizophrenia: Implications of DNA Methylation in Glial Cells.
复制标题
精神分裂症潜在发病机制的进展：神经胶质细胞 DNA 甲基化的影响
DOI：
10.3389/fncel.2015.00451
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发表时间：
2015
影响因子：
5.3
通讯作者：
Xiao L
中科院分区：
文献类型：
--
作者：
Chen XS;Huang N;Michael N;Xiao L
精神分裂症（SZ）是一种慢性和严重的精神疾病，目前没有治愈方法。目前，SZ发病机制的确切分子机制尚不清楚。这种疾病被认为是由遗传、生物、心理和环境因素共同引起的。最近的研究表明，表观遗传调控参与SZ病理。具体而言，DNA甲基化是最早发现的表观遗传修饰之一，已广泛与神经元功能的调节相关，导致精神疾病如SZ。然而，越来越多的证据表明，胶质细胞，特别是功能障碍的少突胶质细胞发生DNA甲基化的变化，有助于SZ的发病机制。本文主要就SZ胶质细胞功能障碍中的DNA甲基化进行综述。阐明这一机制可能会导致开发新的治疗干预策略，通过纠正神经胶质细胞中的异常甲基化来治疗SZ和其他疾病。
Schizophrenia (SZ) is a chronic and severe mental illness for which currently there is no cure. At present, the exact molecular mechanism involved in the underlying pathogenesis of SZ is unknown. The disease is thought to be caused by a combination of genetic, biological, psychological, and environmental factors. Recent studies have shown that epigenetic regulation is involved in SZ pathology. Specifically, DNA methylation, one of the earliest found epigenetic modifications, has been extensively linked to modulation of neuronal function, leading to psychiatric disorders such as SZ. However, increasing evidence indicates that glial cells, especially dysfunctional oligodendrocytes undergo DNA methylation changes that contribute to the pathogenesis of SZ. This review primarily focuses on DNA methylation involved in glial dysfunctions in SZ. Clarifying this mechanism may lead to the development of new therapeutic interventional strategies for the treatment of SZ and other illnesses by correcting abnormal methylation in glial cells.