Cellular Functions of the Amyloid Precursor Protein from Development to Dementia

被引:178
作者
van der Kant, Rik [1 ]
Goldstein, Lawrence S. B. [1 ]
机构
[1] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
关键词
FAMILIAL ALZHEIMERS-DISEASE; APP AXONAL-TRANSPORT; A-BETA; MOUSE MODEL; TERMINAL FRAGMENTS; NEURONAL MIGRATION; SECRETASE ACTIVITY; GAMMA-SECRETASE; BINDING PROTEIN; MICE LACKING;
D O I
10.1016/j.devcel.2015.01.022
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Amyloid precursor protein (APP) is a key player in Alzheimer's disease (AD). The A beta fragments of APP are the major constituent of AD-associated amyloid plaques, and mutations or duplications of the gene coding for APP can cause familial AD. Here we review the roles of APP in neuronal development, signaling, intracellular transport, and other aspects of neuronal homeostasis. We suggest that APP acts as a signaling nexus that transduces information about a range of extracellular conditions, including neuronal damage, to induction of intracellular signaling events. Subtle disruptions of APP signaling functions may be major contributors to AD-causing neuronal dysfunction.
引用
收藏
页码:502 / 515
页数:14
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