Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Islamic Republic of Iran.
Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, P.O. Box 14115-331, Tehran, Islamic Republic of Iran.
Cell Mol Neurobiol. 2017 Nov;37(8):1335-1348. doi: 10.1007/s10571-017-0472-6. Epub 2017 Feb 21.
Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system that results in destruction of the myelin sheath wrapped around the axons and eventual axon degeneration. The disease is pathologically heterogeneous; however, perhaps its most frustrating aspect is the lack of efficient regenerative response for remyelination. Current treatment strategies are based on anti-inflammatory or immunomodulatory medications that have the potential to reduce the numbers of newly evolving lesions. However, therapies are still required that can repair already damaged myelin for which current treatments are not effective. A prerequisite for the development of such new treatments is understanding the reasons for insufficient endogenous repair. This review briefly summarizes the currently suggested causes of remyelination failure in MS and possible solutions.
多发性硬化症（MS）是一种中枢神经系统的慢性免疫介导性疾病，导致包裹在轴突周围的髓鞘被破坏，最终导致轴突变性。这种疾病在病理学上具有异质性；然而，也许最令人沮丧的方面是缺乏有效的再生反应来进行髓鞘修复。目前的治疗策略基于抗炎或免疫调节药物，这些药物有可能减少新出现的病变数量。然而，仍然需要能够修复已经受损的髓鞘的治疗方法，而目前的治疗方法对此并不有效。开发此类新疗法的前提是了解内源性修复不足的原因。这篇综述简要总结了目前认为导致 MS 髓鞘修复失败的原因和可能的解决方案。
