Fawcett James W
Cambridge University Centre for Brain Repair, Cambridge, United Kingdom.
J Neurotrauma. 2006 Mar-Apr;23(3-4):371-83. doi: 10.1089/neu.2006.23.371.
Inhibition by several inhibitory molecules on oligodendrocytes, and by chondroitin sulphate proteoglycans and semaphorins in the glial scar discourages regeneration of axons in the injured spinal cord. This inhibition is compounded by the poor regenerative ability of most central nervous system (CNS) axons. Treatments that block some of these inhibitory mechanisms promote regeneration in animal models of cord injury. Plasticity is also reduced by some of the inhibitory molecules, and some of the treatments that promote regeneration also promote plasticity. This is probably a more achievable therapeutic target than axon regeneration, and an effective treatment would be of assistance to the majority of patients with partial cord injuries.
几种抑制性分子对少突胶质细胞的抑制作用，以及胶质瘢痕中的硫酸软骨素蛋白聚糖和信号素，会阻碍受损脊髓中轴突的再生。大多数中枢神经系统（CNS）轴突再生能力较差，这使得这种抑制作用更加复杂。在脊髓损伤的动物模型中，阻断某些抑制机制的治疗方法可促进再生。一些抑制性分子也会降低可塑性，而一些促进再生的治疗方法也会促进可塑性。这可能是一个比轴突再生更易实现的治疗靶点，有效的治疗方法将有助于大多数部分脊髓损伤的患者。
