Intracellular biology of Alzheimer's disease amyloid beta peptide
Intracellular biology of Alzheimer's disease amyloid beta peptide
复制标题
DOI：
10.1007/s004060050102
复制
发表时间：
1999-12-01
影响因子：
4.7
通讯作者：
Hartmann, T
中科院分区：
文献类型：
--
作者：
Hartmann, T
强有力的证据表明，一种小肽的过量产生与阿尔茨海默病（AD）的发病机制有关。最初，这种肽，β -淀粉样蛋白42 (A β 42)，被认为是由致病事件释放的；现在已经确定，β 42是在阿尔茨海默淀粉样蛋白的正常细胞代谢过程中从细胞中释放出来的。最近，在一系列令人惊讶的报道中，人们发现a β 42是在细胞内产生的，最初可能被认为是少数选定细胞系的奇怪异常，现在已被认为是a β产生的重要细胞途径。此外，分泌和细胞内A β产生的差异可能为AD发病的脑特异性和细胞机制提供线索。
Strong evidence links excess production of a small peptide and the pathogenesis of Alzheimer's disease (AD). Originally this peptide, beta-amyloid 42 (A beta 42), was assumed to be released by a pathogenic event; it is now well established that A beta 42 is released from cells during normal cellular metabolism of the Alzheimer amyloid precursor protein. Recently, in a series of surprising reports it was discovered that A beta 42 is produced intracellularly, and what might have been regarded first as a strange abnormality of a few selected cell lines has now been recognized as an important cellular pathway for A beta production. Moreover, the differences between secretory and intracellular A beta production might hold the clues for brain specificity and cellular mechanisms of AD pathogenesis.