Fas ligand-mediated apoptosis in degenerative disorders of the brain

被引:26
作者
Ethell, DW
Buhler, LA
机构
[1] Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA
[2] Univ Calif Riverside, Grad Program Biochem & Mol Biol, Riverside, CA 92521 USA
关键词
Alzheimer's; apoptosis; EAE; FasL; multiple sclerosis;
D O I
10.1023/A:1025317516396
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
While defective apoptosis predisposes to neoplasia, inappropriate apoptosis in the brain leads to permanent neurological deficits. Disregulated apoptosis has been implicated in several neurodegenerative disorders including Alzheimer's, Parkinson's, and Huntington's diseases. Recent reports have suggested that the key apoptosis regulator Fas ligand (FasL) may participate in both neuronal and immune cell apoptosis in Alzheimer's disease. FasL has also been implicated as a negative regulator for the inflammatory component of the demyelinating brain disorder multiple sclerosis (MS). Here, we discuss how FasL-mediated apoptosis may balance immune cell access to the brain with Alzheimer's disease and MS representing extremes of too little and too much immune access, respectively.
引用
收藏
页码:363 / 370
页数:8
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