少突胶质细胞变性与Alzheimer病  

Oligodendrocyte Degeneration and Alzheimer＇s Disease

作　　者：刘刚[1,2] 陈应柱 赵合庆[1] 包仕尧[1] 

机构地区：[1]苏州大学附属第二医院神经内科,215004 [2]扬州大学临床医学院神经内科,225001

出　　处：《国际脑血管病杂志》2008年第4期317-320,共4页International Journal of Cerebrovascular Diseases

摘　　要：Alzheimer病（AD）是一种重要的神经退行性疾病。最近的证据表明，髓鞘形成和随后的脱失与AD有关，因为晚期产生的少突胶质细胞的独特易损性使髓鞘脱失在AD早期改变中占据核心位置。髓鞘脱失破坏了高度依赖神经冲动同步化的大脑功能，最终导致皮质联合区域功能的断联和随后的神经元脱失。同时，在AD大脑中存在多种使少突胶质细胞变性的机制。因此，阐明其具体机制可帮助更好地了解AD，从而为其治疗提供一定的帮助。Alzhelmer＇s disease （AD） is an important neurodegenerative disease. Recent evidence has indicated that the production and loss of the myelin.sheath are associated with AD because the particular vulnerability of oligodendrocytes produced in the late stage makes the loss of the myelin sheath take a core position in the changes of the earliest stage of AD. The loss of the myelin sheath disrupts synchronization of impulses on which normal brain functions highly depend, and ultimately results in the function disruption of cortical association regions and subsequent neuronal loss. Meanwhile, there are diverse mechanisms that make oligodendrocytes degeneration exist in the brains of AD. Therefore, elucidating its specific mechanism may help better understanding of AD, and thus provide some help for its treatment.

关 键 词：少突胶质细胞 ALZHEIMER病 髓鞘 

分 类 号：R749.16[医药卫生—神经病学与精神病学] R774.6[医药卫生—临床医学]