Kipp Markus
a Steinbeis Research Center - ProMyelo , Aachen , Germany.
b Anatomische Anstalt II, LMU , München , München , Germany.
Expert Rev Neurother. 2016;16(1):1-3. doi: 10.1586/14737175.2016.1116387. Epub 2015 Nov 30.
Remyelination is the natural repair mechanism of demyelination and can be a highly efficient process in multiple sclerosis. However, in the majority of lesions, this regenerative approach is incomplete or fails. It is believed that remyelination protects against progressive axonal damage and thus long-term disability in patients with multiple sclerosis. For this reason, therapeutic promotion of remyelination represents an attractive option for preventing disease progression. In this editorial we casts a critical eye over the most frequently used experimental settings which aim to uncover potential remyelination promoting drugs. This article reflects upon the personal opinion of the author who currently used animal models allow to assess the potency of pharmacological interventions to accelerate, but not to induce myelin repair. Furthermore, it is discussed how remyelination and neuroprotection might well be two separate entities. Thus, induction of remyelination does not necessarily prevent disease progression in multiple sclerosis patients.
髓鞘再生是脱髓鞘的自然修复机制,在多发性硬化症中可能是一个高效的过程。然而,在大多数病变中,这种再生方法是不完全的或失败的。据信,髓鞘再生可防止进行性轴索损伤,从而预防多发性硬化症患者的长期残疾。因此,治疗性促进髓鞘再生是预防疾病进展的一个有吸引力的选择。在这篇社论中,我们对最常用的实验设置进行了批判性审视,这些实验旨在发现潜在的促进髓鞘再生的药物。本文反映了作者的个人观点,即目前使用的动物模型能够评估加速(而非诱导)髓鞘修复的药理干预的效力。此外,还讨论了髓鞘再生和神经保护很可能是两个独立的实体。因此,诱导髓鞘再生不一定能预防多发性硬化症患者的疾病进展。