Dissecting demyelination
Dissecting demyelination
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DOI：
10.1038/nn1995
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发表时间：
2007-11-01
影响因子：
25
通讯作者：
Mi, Sha
中科院分区：
文献类型：
--
作者：
Miller, Robert H.;Mi, Sha
中枢神经系统髓磷脂的丧失和少突胶质细胞髓鞘再生的失败导致功能损伤，这是多发性硬化症等疾病的特征。髓磷脂修复在多发性硬化症中失败的原因目前尚不清楚；然而，对发育过程中少突胶质细胞的产生和髓鞘形成的新认识，以及对髓鞘形成成功的基础的日益了解，正在提供新的见解和治疗靶点。我们认为，成体中枢神经系统髓磷脂修复的成功，概括了与发育过程相关的一系列阶段，而髓磷脂修复的失败，则是由于几个连续事件中任何一个关键过程的扰动。确定髓鞘修复每个阶段的速率限制步骤和最脆弱的方面将为脱髓鞘疾病（如多发性硬化症）的治疗干预提供合乎逻辑的目标。
The loss of central nervous system myelin and the failure of remyelination by oligodendrocytes contribute to the functional impairment that characterizes diseases such as multiple sclerosis. Why myelin repair fails in multiple sclerosis is currently unclear; however, new understanding of the generation of oligodendrocytes and myelination during development, as well as an increasing understanding of the bases of successful remyelination, are providing new insights and therapeutic targets. We propose that successful myelin repair of the adult CNS recapitulates a sequence of stages that generally correlate with those seen during development, whereas unsuccessful myelin repair results from the perturbation of a critical process in any one of several sequential events. Defining the rate-limiting steps and most vulnerable aspects at each stage of myelin repair will provide logical targets for therapeutic intervention in demyelinating diseases such as multiple sclerosis.