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Aberrant DNA methylation profile exacerbates inflammation and neurodegeneration in multiple sclerosis patients.
Journal of Neuroinflammation ( IF 9.3 ) Pub Date : 2020-01-14 , DOI: 10.1186/s12974-019-1667-1
Naiara Celarain 1 , Jordi Tomas-Roig 1
Affiliation  

Multiple sclerosis (MS) is an autoimmune and demyelinating disease of the central nervous system characterised by incoordination, sensory loss, weakness, changes in bladder capacity and bowel function, fatigue and cognitive impairment, creating a significant socioeconomic burden. The pathogenesis of MS involves both genetic susceptibility and exposure to distinct environmental risk factors. The gene x environment interaction is regulated by epigenetic mechanisms. Epigenetics refers to a complex system that modifies gene expression without altering the DNA sequence. The most studied epigenetic mechanism is DNA methylation. This epigenetic mark participates in distinct MS pathophysiological processes, including blood-brain barrier breakdown, inflammatory response, demyelination, remyelination failure and neurodegeneration. In this study, we also accurately summarised a list of environmental factors involved in the MS pathogenesis and its clinical course. A literature search was conducted using MEDLINE through PubMED and Scopus. In conclusion, an exhaustive study of DNA methylation might contribute towards new pharmacological interventions in MS by use of epigenetic drugs.

中文翻译:

异常的 DNA 甲基化谱会加剧多发性硬化症患者的炎症和神经退行性变。

多发性硬化症(MS)是一种中枢神经系统的自身免疫性脱髓鞘疾病,其特征是不协调、感觉丧失、虚弱、膀胱容量和肠道功能改变、疲劳和认知障碍,造成严重的社会经济负担。MS 的发病机制涉及遗传易感性和暴露于不同的环境危险因素。基因与环境的相互作用受到表观遗传机制的调节。表观遗传学是指在不改变 DNA 序列的情况下修改基因表达的复杂系统。研究最多的表观遗传机制是DNA甲基化。这种表观遗传标记参与独特的多发性硬化症病理生理过程,包括血脑屏障破坏、炎症反应、脱髓鞘、髓鞘再生失败和神经变性。在这项研究中,我们还准确总结了 MS 发病机制及其临床过程中涉及的一系列环境因素。通过 PubMED 和 Scopus 使用 MEDLINE 进行文献检索。总之,对 DNA 甲基化的详尽研究可能有助于通过使用表观遗传药物对 MS 进行新的药理学干预。
更新日期:2020-01-14
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