Miron Veronique E, Kuhlmann Tanja, Antel Jack P
Center for Regenerative Medicine, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Biochim Biophys Acta. 2011 Feb;1812(2):184-93. doi: 10.1016/j.bbadis.2010.09.010. Epub 2010 Sep 29.
Myelin is critical in maintaining electrical impulse conduction in the central nervous system. The oligodendrocyte is the cell type responsible for myelin production within this compartment. The mutual supply of trophic support between oligodendrocytes and the underlying axons may indicate why demyelinated axons undergo degeneration more readily; the latter contributes to the neural decline in multiple sclerosis (MS). Myelin repair, termed remyelination, occurs in acute inflammatory lesions in MS and is associated with functional recovery and clinical remittances. Animal models have demonstrated that remyelination is mediated by oligodendrocyte progenitor cells (OPCs) which have responded to chemotactic cues, migrated into the lesion, proliferated, differentiated into mature oligodendrocytes, and ensheathed demyelinated axons. The limited remyelination observed in more chronic MS lesions may reflect intrinsic properties of neural cells or extrinsic deterrents. Therapeutic strategies currently under development include transplantation of exogenous OPCs and promotion of remyelination by endogenous OPCs. All currently approved MS therapies are aimed at dampening the immune response and are not directly targeting neural processes.
髓磷脂对于维持中枢神经系统中的电冲动传导至关重要。少突胶质细胞是负责在该区域内产生髓磷脂的细胞类型。少突胶质细胞与下层轴突之间营养支持的相互供应可能表明为什么脱髓鞘轴突更容易发生变性;后者导致了多发性硬化症(MS)中的神经功能衰退。髓磷脂修复,即髓鞘再生,发生在MS的急性炎症性病变中,并与功能恢复和临床缓解相关。动物模型表明,髓鞘再生由少突胶质前体细胞(OPC)介导,这些细胞对趋化信号作出反应,迁移到病变部位,增殖,分化为成熟的少突胶质细胞,并包裹脱髓鞘轴突。在更慢性的MS病变中观察到的有限的髓鞘再生可能反映了神经细胞的内在特性或外在阻碍因素。目前正在开发的治疗策略包括外源性OPC的移植以及内源性OPC促进髓鞘再生。目前所有获批的MS疗法都旨在抑制免疫反应,而不是直接针对神经过程。