Intraneuronal β-amyloid is a major risk factor -: Novel evidence from the APP/PS1KI mouse model

被引：23

作者：

Bayer, Thomas A. ^{[1
]}

Breyhan, Henning ^{[1
]}

Duan, Kailai ^{[2
]}

Rettig, Jens ^{[2
]}

Wirths, Oliver ^{[1
]}

机构：

[1] Univ Gottingen, Dept Psychiat, Div Mol Psychiat, DE-37075 Gottingen, Germany

[2] Univ Saarland, Inst Physiol, D-6650 Homburg, Germany

来源：

NEURODEGENERATIVE DISEASES | 2008年 / 5卷 / 3-4期

关键词：

intraneuronal beta-amyloid; transgenic mouse; neuron loss; working memory; synaptic plasticity; Alzheimer's disease;

D O I：

10.1159/000113684

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Accumulating evidence points to an important role of intraneuronal P-amyloid (AP) in the development of Alzheimer's disease (AD), with its typical clinical symptoms like memory impairment and changes in personality. We have previously reported on the A beta precursor protein and presenilin-1 knock-out (APP/PS1KI) mouse model with abundant intraneuronal A beta(42) accumulation and a 50% loss of CA1 neurons at 10 months of age. In addition, we observed reduced short- and long-term synaptic plasticity, hippocampal neuron loss, and reduced performance in a working Memory task. These observations support a pivotal role of intraneuronal AP accumulation as a principal pathological trigger in AD. Copyright (c) 2008 S. Karger AG, Basel.

引用

页码：140 / 142

页数：3

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