APOPTOSIS IS INDUCED BY BETA-AMYLOID IN CULTURED CENTRAL-NERVOUS-SYSTEM NEURONS
APOPTOSIS IS INDUCED BY BETA-AMYLOID IN CULTURED CENTRAL-NERVOUS-SYSTEM NEURONS
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DOI：
10.1073/pnas.90.17.7951
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发表时间：
1993-09-01
影响因子：
11.1
通讯作者：
COTMAN, CW
中科院分区：
文献类型：
--
作者：
LOO, DT;COPANI, A;COTMAN, CW
阿尔茨海默病神经退行性变的分子机制尚不清楚；然而，越来越多的证据表明-淀粉样蛋白肽（AbetaP）有助于这种变性。我们现在报道合成的AbetaPs通过激活凋亡通路触发培养神经元的变性。AbetaPs处理的神经元表现出凋亡的形态学和生化特征，包括膜泡、核染色质压实和核小体间DNA断裂。金羧酸是一种核酸酶抑制剂，可防止DNA断裂并延缓细胞死亡。我们的体外实验结果表明，细胞凋亡可能在阿尔茨海默病相关的神经元丧失中发挥作用。
The molecular mechanism responsible for the neurodegeneration in Alzheimer disease is not known; however, accumulating evidence suggests that beta-amyloid peptide (AbetaP) contributes to this degeneration. We now report that synthetic AbetaPs trigger the degeneration of cultured neurons through activation of an apoptotic pathway. Neurons treated with AbetaPs exhibit morphological and biochemical characteristics of apoptosis, including membrane blebbing, compaction of nuclear chromatin, and internucleosomal DNA fragmentation. Aurintricarboxylic acid, an inhibitor of nucleases, prevents DNA fragmentation and delays cell death. Our in vitro results suggest that apoptosis may play a role in the neuronal loss associated with Alzheimer disease.