Activation of Calpain and Caspase Pathways in Demyelination and Neurodegeneration in Animal Model of Multiple Sclerosis
Activation of Calpain and Caspase Pathways in Demyelination and Neurodegeneration in Animal Model of Multiple Sclerosis
复制标题
DOI：
10.2174/187152708784936699
复制
发表时间：
2008-06-01
影响因子：
3
通讯作者：
Banik, Naren L.
中科院分区：
文献类型：
--
作者：
Das, Arabinda;Guyton, M. Kelly;Banik, Naren L.
实验性自身免疫性脑脊髓炎（EAE）是一种广泛认可的多发性硬化症（MS）动物模型，对于研究中枢神经系统（CNS）中的炎症、脱髓鞘和神经变性非常有用。EAE与MS表现出许多相似之处，MS是一种影响人类CNS白色物质的慢性炎症性疾病。各种研究表明，EAE是一种特别有用的动物模型，用于了解免疫介导的CNS病理机制以及MS的进行性临床过程。脱髓鞘和轴突功能障碍先前已在MS和EAE中显示，但目前的证据表明，轴突损伤和神经元死亡也会发生，表明这些疾病含有神经退行性成分。最近的研究还表明，钙蛋白酶和半胱天冬酶途径的激活有助于少突胶质细胞和神经元的凋亡性死亡，促进导致神经功能缺损的病理事件。细胞凋亡参与了EAE的疾病调节和疾病促进过程。本文综述了钙蛋白酶和半胱天冬酶途径在引起EAE动物脱髓鞘和神经退行性变中的主要参与。
Experimental autoimmune encephalomyelitis (EAE), a widely recognized animal model of multiple sclerosis (MS), is highly useful for studying inflammation, demyelination, and neurodegeneration in the central nervous system (CNS). EAE exhibits many similarities with MS, which is a chronic inflammatory disease affecting CNS white matter in humans. Various studies have indicated that EAE is a particularly useful animal model for understanding both the mechanisms of immune-mediated CNS pathology and also the progressive clinical course of MS. Demyelination and axonal dysfunction have previously been shown in MS and EAE but current evidences indicate that axonal damage and neuron death also occur, demonstrating that these diseases harbor a neurodegenerative component. Recent studies also have shown that the activation of calpain and caspase pathways contribute to the apoptotic death of oligodendrocytes and neurons, promoting the pathological events leading to neurological deficits. Apoptosis is involved in the disease-regulating as well as in the disease-promoting processes in EAE. This review discusses the major involvement of calpain and caspase pathways in causing demyelination and neurodegeneration in EAE animals.