Buzzard Katherine, Chan Wing Hei, Kilpatrick Trevor, Murray Simon
Department of Neurology, Royal Melbourne Hospital, Parkville, VIC, 3050, Australia.
Department of Anatomy and Neuroscience, The University of Melbourne, Parkville, VIC, 3010, Australia.
Adv Neurobiol. 2017;15:211-252. doi: 10.1007/978-3-319-57193-5_8.
Multiple sclerosis (MS) is the most common neurodegenerative disease affecting young adults in our community. It is a complex disease influenced by gender, genetic and environmental factors. MS is a chronic inflammatory disease of the central nervous system caused by aberrant immune activation resulting in damage to myelin sheaths within the brain and spinal cord and axonal loss. The demyelinating insult initially impairs the speed and efficiency of nerve cell function. In the majority of cases, this is followed by an innate endogenous repair response that can restore the myelin sheath and nerve cell function to relatively normal levels. However over time and with subsequent demyelinating events, this capacity is lost ultimately leading to neural degeneration. The influences that oligodendrocytes and myelin exert upon nerve cells to sustain their health and viability have begun to be identified. While immune-directed therapies can reduce the frequency of relapses and development of new lesions, they have little effect upon remyelination and nerve cell repair. This presents the next big challenge in MS therapeutics; complementing immune targeted therapies with strategies that directly target the primary cause of disability, that of remyelination.
多发性硬化症（MS）是我们社区中影响年轻人的最常见神经退行性疾病。它是一种受性别、遗传和环境因素影响的复杂疾病。MS是一种中枢神经系统的慢性炎症性疾病，由异常免疫激活引起，导致脑和脊髓内的髓鞘损伤以及轴突丢失。脱髓鞘损伤最初会损害神经细胞功能的速度和效率。在大多数情况下，随后会出现一种先天性内源性修复反应，可将髓鞘和神经细胞功能恢复到相对正常的水平。然而，随着时间的推移以及随后的脱髓鞘事件，这种能力会丧失，最终导致神经退化。少突胶质细胞和髓鞘对神经细胞维持其健康和活力所产生的影响已开始得到确认。虽然免疫导向疗法可以减少复发频率和新病灶的形成，但它们对髓鞘再生和神经细胞修复几乎没有作用。这是MS治疗中的下一个重大挑战；用直接针对导致残疾的主要原因（即髓鞘再生）的策略来补充免疫靶向疗法。
