Epigenetic mechanisms in multiple sclerosis: implications for pathogenesis and treatment

被引:101
作者
Huynh, Jimmy L. [1 ,2 ]
Casaccia, Patrizia [1 ,2 ,3 ]
机构
[1] Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA
[2] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY 10029 USA
[3] Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA
关键词
MYELIN BASIC-PROTEIN; LONG NONCODING RNA; DNA METHYLATION; HISTONE ACETYLATION; OLIGODENDROCYTE DIFFERENTIATION; ENVIRONMENTAL-FACTORS; ARGININE METHYLATION; CHROMATIN-STRUCTURE; GENE-EXPRESSION; NUCLEAR EXPORT;
D O I
10.1016/S1474-4422(12)70309-5
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Clinical neurologists and scientists who study multiple sderosis face open questions regarding the integration of epidemiological data with genome-wide association studies and clinical management. of patients. It is becoming evident that the interplay of environmental influences and individual genetic susceptibility modulates disease presentation and therapeutic responsiveness. The molecular mechanisms through which environmental signals are translated into changes in gene expression include DNA methylation, post-translational modification of nudeosomal histones, and non-coding RNAs. These mechanisms are regulated by families of specialised enzymes that are tissue selective and cell-type specific. A model of multiple sclerosis pathogenesis should integrate underlying risk related to genetic susceptibility with cell-type specific epigenetic changes occurring in the immune system and in the brain in response to ageing and environmental stimuli.
引用
收藏
页码:195 / 206
页数:12
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