APP physiological and pathophysiological functions： insights from animal models  

作　　者：Qinxi Guo Zilai Wang Hongmei Li Mary Wiese Hui Zheng 

机构地区：[1]Huffington Center on Aging, Baylor College of Medicine, One Baylor Plaza, BCM：MS230, Houston, TX 77030, USA [2]Program in Translational Biology and Molecular Medicine, Houston, TX 77030, USA [3]Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA

出　　处：《Cell Research》2012年第1期78-89,共12页细胞研究（英文版）

摘　　要：The amyloid precursor protein （APP） has been under intensive study in recent years, mainly due to its critical role in the pathogenesis of Alzheimer＇s disease （AD）. β-Amyloid （Aβ） peptides generated from APP proteolytic cleavage can aggregate, leading to plaque formation in human AD brains. Point mutations of APP affecting Aβ production are found to be causal for hereditary early onset familial AD. It is very likely that elucidating the physiological proper- ties of APP will greatly facilitate the understanding of its role in AD pathogenesis. A number of APP loss- and gain- of-function models have been established in model organisms including Caenorhabditis elegans, Drosophila, zebrafish and mouse. These in vivo models provide us valuable insights into APP physiological functions. In addition, several knock-in mouse models expressing mutant APP at a physiological level are available to allow us to study AD patho- genesis without APP overexpression. This article will review the current physiological and pathophysiological animal models of APP.

关 键 词：Alzheimer＇s disease APP AΒ KNOCK-IN animal models 

分 类 号：Q510.3[生物学—生物化学] TS202.3[轻工技术与工程—食品科学]