Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Neurochemistry Laboratory, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Neurotherapeutics. 2018 Jan;15(1):156-175. doi: 10.1007/s13311-017-0593-0.
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.
S-腺苷甲硫氨酸(SAMe)作为主要的甲基供体,通过细胞转甲基途径,包括 DNA、组蛋白、蛋白磷酸酶 2A 和几种儿茶酚胺部分的甲基化,对中枢神经系统功能发挥影响。基于现有证据,本综述重点关注一生中严重的神经精神和神经退行性疾病及其相关神经病理学,这些疾病与 SAMe 产生的缺乏/负荷和转甲基途径的紊乱有关。本综述还包括 SAMe 在每个年龄组治疗这些疾病中的当前应用。