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Abstract：
Multiple sclerosis (MS) is an autoimmune and inflammatory disorder affecting the central nervous system whose cause is still largely unknown. Oligodendrocyte degeneration results in demyelination of axons, which can eventually be repaired by a mechanism called remyelination. Prevention of demyelination and the pharmacological support of remyelination are two promising strategies to ameliorate disease progression in MS patients. The cuprizone model is commonly employed to investigate oligodendrocyte degeneration mechanisms or to explore remyelination pathways. During the last decades, several different protocols have been applied, and all have their pros and cons. This article intends to offer guidance for conducting pre-clinical trials using the cuprizone model in mice, focusing on discovering new treatment approaches to prevent oligodendrocyte degeneration or enhance remyelination.
摘要：
多发性硬化症（MS）是一种影响中枢神经系统的自身免疫性和炎症性疾病，其原因尚不清楚。少突胶质细胞变性导致轴突脱髓鞘，最终可以通过一种叫做髓鞘再生的机制来修复。预防脱髓鞘和药物支持髓鞘再生是改善MS患者疾病进展的两种有希望的策略。铜松模型通常用于研究少突胶质细胞变性机制或探索髓鞘再生途径。在过去的几十年里，已经应用了几种不同的协议，都有自己的优点和缺点。本文旨在为使用Cuprizone模型在小鼠中进行临床前试验提供指导。专注于发现新的治疗方法，以防止少突胶质细胞变性或增强髓鞘再生。
