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S-Adenosyl Methionine and Transmethylation Pathways in Neuropsychiatric Diseases Throughout Life

机译:终生神经精神疾病中的S-腺苷蛋氨酸和甲基转移途径

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摘要

S-Adenosyl methionine (SAMe), as a major methyl donor, exerts its influence on central nervous system function through cellular transmethylation pathways, including the methylation of DNA, histones, protein phosphatase 2A, and several catecholamine moieties. Based on available evidence, this review focuses on the lifelong range of severe neuropsychiatric and neurodegenerative diseases and their associated neuropathologies, which have been linked to the deficiency/load of SAMe production or/and the disturbance in transmethylation pathways. Also included in this review are the present-day applications of SAMe in the treatment in these diseases in each age group.Electronic supplementary materialThe online version of this article (10.1007/s13311-017-0593-0) contains supplementary material, which is available to authorized users.
机译:作为主要的甲基供体,S-腺苷甲硫氨酸(SAMe)通过细胞的甲基化途径对中枢神经系统功能产生影响,包括DNA,组蛋白,蛋白质磷酸酶2A和几个儿茶酚胺部分的甲基化。根据现有证据,本综述重点研究严重神经精神疾病和神经退行性疾病及其相关神经病理的终生范围,这些疾病与SAMe产生/负荷不足或/和甲基化途径障碍相关。该评价还包括SAMe在各个年龄段的这些疾病的治疗中的最新应用。电子补充材料本文的在线版本(10.1007 / s13311-017-0593-0)包含补充材料,可以通过以下途径获得给授权用户。

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