Targeting oligodendrocyte protection and remyelination in multiple sclerosis.
Targeting oligodendrocyte protection and remyelination in multiple sclerosis.
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DOI：
10.1002/msj.20244
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发表时间：
2011-03
影响因子：
--
通讯作者：
John, Gareth R.
中科院分区：
文献类型：
--
作者：
Zhang, Jingya;Kramer, Elisabeth G.;Mahase, Sean;Dutta, Dipankar J.;Bonnamain, Virginie;Argaw, Azeb T.;John, Gareth R.
多发性硬化症（MS）是一种脑和脊髓的炎性脱髓鞘疾病，推测其病因为自身免疫性。脱髓鞘轴突传导阻滞是早期神经症状的基础，而轴突横断被认为是造成更永久性的后期缺陷的原因。批准的疾病治疗是免疫调节性的，并降低病变形成和临床恶化的速度，但在预防MS患者的残疾发作方面仅部分有效。直接保护产生髓鞘的少突胶质细胞和促进髓鞘再生的方法可能会改善长期预后并降低轴突横断率。在转基因动物中的研究提高了我们对MS模型中CNS病理学机制的理解，并确定了调节少突胶质细胞活力和髓鞘修复的途径。然而，虽然临床试验正在进行中，许多都是不成功的，尚未批准的治疗目标在MS这些领域。在这篇综述中，我们研究的途径少突胶质细胞的保护和内源性髓鞘修复的脱髓鞘和髓鞘再生的动物模型，其相关性作为治疗人类患者。
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the brain and spinal cord with a presumed autoimmune etiology. Conduction block in demyelinated axons underlies early neurological symptoms, whereas axonal transection is believed responsible for more permanent later deficits. Approved treatments for the disease are immunoregulatory, and reduce the rate of lesion formation and clinical exacerbation, but are only partially effective in preventing the onset of disability in MS patients. Approaches that directly protect myelin-producing oligodendrocytes and enhance remyelination may improve long-term outcomes and reduce the rate of axonal transection. Studies in genetically modified animals have improved our understanding of mechanisms underlying CNS pathology in MS models, and have identified pathways that regulate oligodendrocyte viability and myelin repair. However, although clinical trials are ongoing, many have been unsuccessful and no treatments are yet approved that target these areas in MS. In this review, we examine avenues for oligodendrocyte protection and endogenous myelin repair in animal models of de- and remyelination, and their relevance as therapeutics in human patients.
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影响因子：
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