Ehling Rainer, Berger Thomas, Reindl Markus
Clinical Department of Neurology, Innsbruck Medical University, Austria.
Cent Nerv Syst Agents Med Chem. 2010 Mar;10(1):3-15. doi: 10.2174/187152410790780127.
Multiple sclerosis (MS) is the most common disabling neurological disease in young adults characterized by recurrent relapses and / or progression that are attributable to multifocal inflammation, demyelination and axonal pathology within the central nervous system. Currently approved disease-modifying treatments achieve their effects primarily by blocking the proinflammatory response in a nonspecific manner. Their limited clinical efficacy urges a more differentiated and specific therapeutic approach. Advances in understanding the pathophysiology of MS and appreciation of the contribution of neurodegenerative processes to disease pathology have led to promising therapeutic approaches at different points along the MS disease pathway: (i) monoclonal antibody therapy has provided the opportunity to rationally direct the therapeutic intervention by specifically targeting mechanisms of the immune system such as CD52 (alemtuzumab), CD25 (daclizumab), VLA-4 (natalizumab) and CD20 (rituximab); (ii) novel oral immunomodulating agents have shown to prevent lymphocyte recirculation from lymphoid organs such as fingolimod (FTY720); (iii) blocking of intracellular signaling cascades or ion channels at the cell-surface can protect axons from degeneration and restore axonal function in experimental settings; (iv) neuroprotective agents and stem cell therapy are able to promote remyelination and axonal regeneration in vitro. Despite the tremendous efforts undertaken, a better understanding of the sequential evolution of the MS lesion and the development of clinical surrogate markers, which allow to define subsets of patients with different forms of underlying pathogenesis, is necessary. This will pave the way for an optimized treatment approach, which will likely need both to target inflammation and to focus on promotion of neuroprotection and repair.
多发性硬化症(MS)是年轻成年人中最常见的致残性神经疾病,其特征为复发和/或病情进展,这归因于中枢神经系统内的多灶性炎症、脱髓鞘和轴突病变。目前获批的疾病修正治疗主要通过非特异性阻断促炎反应来发挥作用。其有限的临床疗效促使人们寻求更具针对性和特异性的治疗方法。对MS病理生理学的深入理解以及对神经退行性过程在疾病病理中作用的认识,已在MS疾病进程的不同阶段带来了有前景的治疗方法:(i)单克隆抗体疗法通过特异性靶向免疫系统机制,如CD52(阿仑单抗)、CD25(达利珠单抗)、VLA-4(那他珠单抗)和CD20(利妥昔单抗),为合理指导治疗干预提供了机会;(ii)新型口服免疫调节剂已显示可防止淋巴细胞从淋巴器官再循环,如芬戈莫德(FTY720);(iii)在实验环境中,阻断细胞内信号级联或细胞表面离子通道可保护轴突免于退化并恢复轴突功能;(iv)神经保护剂和干细胞疗法能够在体外促进髓鞘再生和轴突再生。尽管付出了巨大努力,但仍有必要更好地理解MS病变的连续演变以及开发临床替代标志物,以定义具有不同潜在发病机制形式的患者亚组。这将为优化治疗方法铺平道路,该方法可能既需要针对炎症,又需要专注于促进神经保护和修复。