Apoptosis in multiple sclerosis - etiopathogenetic relevance and perspectives for new therapeutic strategies

被引:0
|
作者
Aktas, O [1 ]
Wendling, U [1 ]
Zschenderlein, R [1 ]
Zipp, F [1 ]
机构
[1] Humboldt Univ, Fak Med, Neurol Klin & Poliklin, D-1040 Berlin, Germany
来源
NERVENARZT | 2000年 / 71卷 / 10期
关键词
multiple sclerosis; apoptosis; immunopathogenesis; CD95; TNF;
D O I
10.1007/s001150050664
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Apoptosis, or programmed cell death, is a physiological cell suicide program mainly leading to selective elimination of useless cells. This mechanism is important for the homeostasis of the immune system and presumably plays a two-sided role in the pathogenesis of multiple sclerosis (MS). On the one hand, evidence has been provided that impaired apoptosis might result in increased numbers or persistence of activated myelin-specifier cells, thus inducing the pathophysiologic processes in MS. On the other hand, local tissue damage might involve apoptosis of glial and neuronal cells and lead to the clinical symptoms. Here, an overview is presented on the current knowledge of the role of apoptosis in the pathogenesis of MS, and implications for related therapeutic strategies are discussed.
引用
收藏
页码:767 / 773
页数:9
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