Dubois-Dalcq M, Armstrong R
Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892.
Bioessays. 1990 Dec;12(12):569-76. doi: 10.1002/bies.950121203.
Central nervous system (CNS)* regeneration is a subject of great interest, particularly in diseases causing a dramatic loss of neurons. However, some CNS diseases do not affect neurons but damage other cells, such as the myelin-forming cells--called oligodendrocytes--which are also crucial to the harmonious function of the nervous system. Diseases in which oligodendrocytes and myelin are attacked can cause devastating neurological dysfunction which is sometimes followed by recovery and myelin repair or remyelination. The question of the regeneration potential of oligodendrocytes in experimental and human demyelinating diseases such as multiple sclerosis has been debated for a long time. Present evidence suggests that oligodendrocyte precursor cells persist in the adult CNS and that oligodendrocyte regeneration can occur but may be limited by ongoing disease processes. Here we will briefly review recent advances which have broadened our understanding of the cellular and molecular events of CNS remyelination.
中枢神经系统（CNS）*再生是一个备受关注的课题，尤其是在导致神经元大量丧失的疾病中。然而，一些中枢神经系统疾病并不影响神经元，而是损害其他细胞，例如形成髓鞘的细胞——称为少突胶质细胞——它们对神经系统的和谐功能也至关重要。少突胶质细胞和髓鞘受到攻击的疾病会导致严重的神经功能障碍，有时随后会出现恢复以及髓鞘修复或髓鞘再生。在实验性和人类脱髓鞘疾病（如多发性硬化症）中，少突胶质细胞的再生潜力问题已经争论了很长时间。目前的证据表明，少突胶质前体细胞在成年中枢神经系统中持续存在，并且少突胶质细胞再生可以发生，但可能受到持续疾病进程的限制。在这里，我们将简要回顾最近的进展，这些进展拓宽了我们对中枢神经系统髓鞘再生的细胞和分子事件的理解。
