Stangel Martin, Trebst Corinna
Department of Neurology, Medical School Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
Curr Neurol Neurosci Rep. 2006 May;6(3):229-35. doi: 10.1007/s11910-006-0010-2.
Spontaneous remyelination and repair mechanisms in multiple sclerosis are mostly insufficient and contribute to clinical disability. Treatments improving these processes are not yet available but basic research in animal models has led to the proposal of several repair strategies. These include enhancement of the naturally occurring mechanisms, remyelination due to a change of the immune response, and transfer of myelinating cells. Despite the encouraging experimental findings and the constantly increasing knowledge of the molecular mechanisms of remyelination and remyelination failure, there remain many questions before this knowledge can be successfully translated into clinical trials.
多发性硬化症中的自发髓鞘再生和修复机制大多不足，是导致临床残疾的原因之一。目前尚无改善这些过程的治疗方法，但动物模型的基础研究已提出了几种修复策略。这些策略包括增强自然发生的机制、因免疫反应改变而实现的髓鞘再生以及髓鞘形成细胞的移植。尽管实验结果令人鼓舞，且对髓鞘再生和髓鞘再生失败的分子机制的了解不断增加，但在将这些知识成功转化为临床试验之前，仍有许多问题有待解决。
