Curtin Health Innovation Research Institute, Curtin University, Bentley, Western Australia, Australia.
Perron Institute for Neurological and Translational Science, Nedlands, Western Australia, Australia.
J Neurotrauma. 2020 Mar 1;37(5):739-769. doi: 10.1089/neu.2019.6890.
Traumatic brain injury (TBI) and spinal cord injury (SCI) present a significant contribution to the global disease burden. White matter tracts are susceptible to both the physical forces of trauma and cascades of pathological secondary degeneration. Oligodendrocytes, the myelinating cells of the central nervous system (CNS), and their precursors are particularly vulnerable cell populations and their disruption results in a loss of white matter, dysmyelination, and poor myelin repair. White matter aberrations in TBI and SCI can be visualized using a number of magnetic resonance imaging (MRI)-based modalities. Recent advances in diffusion MRI allow researchers to investigate subtle abnormalities in white matter microstructure and connectivity, resting state networks, and metabolic perturbations associated with injury. Damage to oligodendroglia underlies white matter aberrations and occurs as a result of glutamate excitotoxicity, intracellular calcium ion (Ca) overload, and oxidative damage to lipids, proteins, and DNA. Structural changes to myelin include myelin decompaction, loosening of myelin lamellae, and disruption to the node of Ranvier complex. Neuronal and functional loss accompany dysmyelination together with an increase in astro- and microgliosis. Remyelination is often partial, and more work is needed to understand deficits in remyelination post-injury to develop strategies to both protect and repair myelin and thereby preserve function. This review covers disruptions to oligodendrocyte function and white matter tract structure in the context of TBI and SCI, with an emphasis on Australian contributions in recognition of the International Neurotrauma Symposium held in Melbourne, Australia in 2020.
创伤性脑损伤（TBI）和脊髓损伤（SCI）对全球疾病负担有重大影响。白质束易受创伤的物理力和病理级联继发性退化的影响。少突胶质细胞是中枢神经系统（CNS）的髓鞘形成细胞及其前体细胞是特别脆弱的细胞群体，其破坏导致白质丢失、脱髓鞘和髓鞘修复不良。TBI 和 SCI 中的白质异常可以使用多种基于磁共振成像（MRI）的方式进行可视化。扩散 MRI 的最新进展使研究人员能够研究与损伤相关的白质微观结构和连接、静息状态网络以及代谢扰动的细微异常。少突胶质细胞的损伤是白质异常的基础，是由于谷氨酸兴奋性毒性、细胞内钙离子（Ca）超载以及脂质、蛋白质和 DNA 的氧化损伤引起的。髓鞘的结构变化包括髓鞘解压缩、髓鞘层松动以及Ranvier 结复合体的破坏。脱髓鞘伴随着神经元和功能丧失，以及星形胶质细胞和小胶质细胞增生增加。少突胶质细胞的再髓鞘化通常是不完全的，需要更多的工作来了解损伤后再髓鞘化的缺陷，以制定保护和修复髓鞘的策略，从而维持功能。本综述涵盖了 TBI 和 SCI 背景下少突胶质细胞功能和白质束结构的破坏，重点介绍了澳大利亚的贡献，以纪念 2020 年在澳大利亚墨尔本举行的国际神经创伤研讨会。
