Multiple Sclerosis Center, Department of Neurology, University of California San Francisco (UCSF), 675 Nelson Rising Lane, 2nd floor, Room 221F, Box 3206, 94158, San Francisco, CA, USA,
CNS Drugs. 2013 Oct;27(10):799-815. doi: 10.1007/s40263-013-0093-7.
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that is pathologically characterized by inflammatory demyelination and neurodegeneration. Axonal damage, along with neuronal loss, occurs from disease onset and may lead to progressive and permanent disability. In contrast with the inflammatory pathways, the molecular mechanisms leading to MS neurodegeneration remain largely elusive. With improved understanding of these mechanisms, new potential therapeutic targets for neuroprotection have emerged. We review the current understanding of neurodegenerative processes at play in MS and discuss potential outcome measures and targets for neuroprotection trials.
多发性硬化症(MS)是一种中枢神经系统脱髓鞘疾病,其病理特征为炎症性脱髓鞘和神经退行性变。从疾病发病开始就存在轴突损伤和神经元丢失,并可能导致进行性和永久性残疾。与炎症途径不同,导致 MS 神经退行性变的分子机制在很大程度上仍难以捉摸。随着对这些机制的深入了解,神经保护的新潜在治疗靶点已经出现。我们回顾了目前对 MS 中发挥作用的神经退行性过程的理解,并讨论了神经保护试验的潜在结果测量和靶点。