Demyelination as a rational therapeutic target for ischemic or traumatic brain injury.
Demyelination as a rational therapeutic target for ischemic or traumatic brain injury.
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脱髓鞘作为缺血性或创伤性脑损伤的合理治疗目标
DOI：
10.1016/j.expneurol.2015.03.017
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发表时间：
2015-10
影响因子：
5.3
通讯作者：
Gao Y
中科院分区：
文献类型：
--
作者：
Shi H;Hu X;Leak RK;Shi Y;An C;Suenaga J;Chen J;Gao Y
以往关于中风和创伤性脑损伤(TBI)的研究主要强调灰质内神经细胞的病理改变。然而，最近的研究强调了白质完整性在这些疾病的长期康复中同样重要。脱髓鞘是白质损伤的主要组成部分，其特征是髓鞘丢失和少突胶质细胞死亡。脱髓鞘对长期感觉运动和认知障碍有重要作用，因为成人大脑只有有限的少突胶质细胞再生和轴突再髓鞘形成能力。本文就急性脑损伤后脱髓鞘和少突胶质细胞死亡的主要原因作一综述，并讨论脱髓鞘过程中髓鞘、轴突、小胶质细胞和星形胶质细胞之间的相互作用。最近发现的调节再髓鞘形成过程的分子可能为恢复脑白质完整性和改善中风或脑外伤患者的长期神经恢复提供新的治疗靶点。
Previous research on stroke and traumatic brain injury (TBI) heavily emphasized pathological alterations in neuronal cells within gray matter. However, recent studies have highlighted the equal importance of white matter integrity in long-term recovery from these conditions. Demyelination is a major component of white matter injury and is characterized by loss of the myelin sheath and oligodendrocyte cell death. Demyelination contributes significantly to long-term sensorimotor and cognitive deficits because the adult brain only has limited capacity for oligodendrocyte regeneration and axonal remyelination. In the current review, we will provide an overview of the major causes of demyelination and oligodendrocyte cell death following acute brain injuries, and discuss the crosstalk between myelin, axons, microglia, and astrocytes during the process of demyelination. Recent discoveries of molecules that regulate the processes of remyelination may provide novel therapeutic targets to restore white matter integrity and improve long-term neurological recovery in stroke or TBI patients.