Alzheimer's disease sends the wrong signals - a perspective

被引：10

作者：

Neve, Rachael L. ^{[1
]}

机构：

[1] McLean Hosp, Belmont, MA 02478 USA

来源：

AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS | 2008年 / 15卷 / 01期

关键词：

Alzheimer's disease; signaling; presenilin; amyloid precursor protein;

D O I：

10.1080/13506120701814608

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Familial Alzheimer's disease mutations in presenilin and the amyloid precursor protein (APP) are thought to cause Alzheimer's disease (AD) neurodegeneration by increasing production and aggregation of amyloid beta (A). However, presenilin has functions that are distinct from its role in the -secretase complex, while APP has signaling functions that transcend its role as the source of A. Three recent papers highlight the potential importance of presenilin and APP signaling in the etiology of AD.

引用

页码：1 / 4

页数：4

共 22 条

[21] Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration [J].