Dutta Ranjan, Trapp Bruce D
Department of Neuroscience, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Neurology. 2007 May 29;68(22 Suppl 3):S22-31; discussion S43-54. doi: 10.1212/01.wnl.0000275229.13012.32.
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS. Approximately 2 million people worldwide have MS, with females outnumbering males 2:1. Because of its high prevalence, MS is the leading cause of nontraumatic neurologic disability in young adults in the United States and Europe. Axon loss is the major cause of irreversible disability in patients with MS. Axon damage, including transection of the axon, begins early in MS and correlates with inflammatory activity. Several mechanisms lead to axon loss, including inflammatory secretions, loss of myelin-derived support, disruption of axonal ion concentrations, energy failure, and Ca(2+) accumulation. Therapeutic interventions directed toward each of these mechanisms need to be tested for their efficacy in enhancing axon survival and, ultimately, their ability to delay progression of neurologic disability in patients with MS.
多发性硬化症(MS)是一种中枢神经系统的慢性炎症性脱髓鞘疾病。全球约有200万人患有MS,女性患者数量是男性的2倍。由于其高患病率,MS是美国和欧洲年轻人非创伤性神经残疾的主要原因。轴突损失是MS患者不可逆残疾的主要原因。轴突损伤,包括轴突横断,在MS早期就开始了,并且与炎症活动相关。有几种机制会导致轴突损失,包括炎症分泌物、髓鞘衍生支持的丧失、轴突离子浓度的破坏、能量衰竭和Ca(2+)积累。针对这些机制的治疗干预措施需要测试其在提高轴突存活率方面的疗效,以及最终在延缓MS患者神经残疾进展方面的能力。