Remyelination in multiple sclerosis: Cellular mechanisms and novel therapeutic approaches
Remyelination in multiple sclerosis: Cellular mechanisms and novel therapeutic approaches
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DOI：
10.1002/jnr.23493
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发表时间：
2015-05
影响因子：
4.2
通讯作者：
J. Olsen;E. Akirav
中科院分区：
文献类型：
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作者：
J. Olsen;E. Akirav
覆盖轴突的髓鞘允许电脉冲在神经系统中快速传播。少突胶质细胞（OD）是中枢神经系统（CNS）中产生髓磷脂的细胞，负责包裹神经元的轴突。多发性硬化症 (MS) 是一种中枢神经系统脱髓鞘疾病，可通过白质和灰质病变来识别。这些病变由因髓磷脂和 OD 的自身免疫反应而失去髓磷脂的轴突组成。目前多发性硬化症的治疗主要针对该疾病的自身免疫方面。然而，这些免疫调节剂并不直接增强髓鞘再生过程。神经祖细胞可以分化为 OD 并替代丢失的髓鞘，从而增强髓鞘再生能力，尽管成功的髓鞘再生很复杂并且依赖于多种因素。恢复丢失的髓磷脂可能会保护轴突免于退化，并恢复多发性硬化症患者冲动的最佳传导，需要对髓鞘形成前疗法进行进一步研究。免疫调节剂和髓鞘再生增强剂的组合可能是许多多发性硬化症患者的最佳治疗方案。本综述讨论了多发性硬化症中的脱髓鞘、髓鞘再生机制以及目前旨在促进多发性硬化症患者髓鞘再生的治疗方法。 © 2014 Wiley 期刊公司。
The myelin sheath that coats axons allows rapid propagation of electrical impulses across the nervous system. Oligodendrocytes (ODs) are myelin‐producing cells of the central nervous system (CNS) responsible for wrapping the axons of neurons. Multiple sclerosis (MS) is a demyelinating disease of the CNS identifiable by white and gray matter lesions. These lesions consist of axons that have lost their myelin through an autoimmune response to myelin and ODs. Current treatments for MS target the autoimmune aspect of the disease. However, these immunomodulators do not directly enhance the process of remyelination. The ability to remyelinate lesions can be enhanced by neural progenitor cells that can differentiate into ODs and replace lost myelin, although successful remyelination is complex and dependent on multiple factors. The restoration of lost myelin might protect the axon from degeneration and restore optimal conduction of impulses in MS patients, requiring further research on proremyelinating therapies. The combination of immunomodulators and remyelinating enhancers might be the best course of treatment for many MS patients. This Review discusses demyelination in MS, the mechanisms of remyelination, and current therapies designed to promote remyelination in MS patients. © 2014 Wiley Periodicals, Inc.