Lisak Robert P
Division of Neuroimmunology, Department of Neurology, Wayne State University School of Medicine and the Detroit Medical Center, Detroit, Michigan 48201, USA.
Neurology. 2007 May 29;68(22 Suppl 3):S5-12; discussion S43-54. doi: 10.1212/01.wnl.0000275227.74893.bd.
It is increasingly apparent that neurodegeneration in multiple sclerosis (MS) begins earlier in the course of the disease than was previously believed. The loss of axons, which results in permanent deficits, is distributed beyond regions of abnormal-appearing CNS white matter, and a constant background of neuron loss continues to take place while clinical symptoms wax and wane. It is therefore important to precisely define the scope of neurodegeneration so that experimental and clinical approaches to providing neuroprotective therapies can be devised that will halt and reverse neuron damage. Some of the complexities involved in cellular interactions in the normal-appearing and obviously affected CNS are reviewed here as a starting point for the consideration of approaches to neuroprotective strategies.
越来越明显的是，多发性硬化症（MS）中的神经退行性变在疾病进程中比之前认为的开始得更早。导致永久性缺陷的轴突损失分布在中枢神经系统（CNS）外观异常的白质区域之外，并且在临床症状波动期间，神经元损失的持续背景仍在继续。因此，精确界定神经退行性变的范围很重要，以便能够设计出提供神经保护疗法的实验和临床方法，从而阻止并逆转神经元损伤。本文回顾了正常外观和明显受影响的中枢神经系统中细胞相互作用所涉及的一些复杂性，作为考虑神经保护策略方法的起点。
