Fas ligand-mediated apoptosis in degenerative disorders of the brain
Fas ligand-mediated apoptosis in degenerative disorders of the brain
复制标题
DOI：
10.1023/a:1025317516396
复制
发表时间：
2003-09-01
影响因子：
9.1
通讯作者：
Buhler, LA
中科院分区：
文献类型：
--
作者：
Ethell, DW;Buhler, LA
虽然有缺陷的细胞凋亡易患肿瘤，但脑中不适当的细胞凋亡会导致永久性神经功能缺损。失调的细胞凋亡与包括阿尔茨海默病、帕金森病和亨廷顿病在内的几种神经退行性疾病有关。近年来的研究表明，凋亡调节因子Fas配体（FasL）可能参与了阿尔茨海默病神经细胞和免疫细胞的凋亡。FasL也被认为是脱髓鞘脑疾病多发性硬化症（MS）的炎症组分的负调节剂。在这里，我们讨论了FasL介导的细胞凋亡如何平衡免疫细胞进入大脑与阿尔茨海默病和MS代表极端的太少和太多的免疫访问，分别。
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.