Kreitman Rivka Riven, Blanchette François
Teva Neuroscience, 1090 Horsham Road, North Wales, PA 19454-1090, USA.
Mult Scler. 2004 Jun;10 Suppl 1:S81-6; discussion S86-9. doi: 10.1191/1352458504ms1037oa.
Inflammation and neurodegeneration characterize the pathogenesis of multiple sclerosis (MS). Slow axonal degeneration, rather than acute inflammation, is considered the cause of chronic disability in MS. The signs of acute axonal damage and loss have been shown to occur early in the lesion development of patients with chronic MS and often correlate with demyelination and inflammation. While immune activity in the central nervous system has traditionally been considered to be a detrimental event in MS, recent studies have found that autoimmune T cells may play an important role in protecting neurons from the ongoing spreading damage. Neuroprotection in MS is a new and evolving concept, and many questions remain with regard to potential targets for therapeutic intervention. Preliminary studies, both in animals and in humans, have suggested that glatiramer acetate (GA) may confer neuroprotective activity in addition to bystander suppression. Additional research is needed to determine if these promising neuroprotective effects correlated with the long-term effect of GA in MS.
炎症和神经退行性变是多发性硬化症（MS）发病机制的特征。轴突缓慢退化而非急性炎症被认为是MS慢性残疾的原因。急性轴突损伤和丢失的迹象已被证明在慢性MS患者的病变发展早期就会出现，并且通常与脱髓鞘和炎症相关。虽然传统上认为中枢神经系统中的免疫活动在MS中是有害事件，但最近的研究发现自身免疫性T细胞可能在保护神经元免受持续扩散损伤方面发挥重要作用。MS中的神经保护是一个新的且不断发展的概念，关于治疗干预的潜在靶点仍有许多问题。动物和人体的初步研究表明，醋酸格拉替雷（GA）除了具有旁观者抑制作用外，可能还具有神经保护活性。需要进一步研究以确定这些有前景的神经保护作用是否与GA对MS的长期疗效相关。
