Behavioral deficits in APPV717F transgenic mice deficient for the apolipoprotein E gene

被引:29
作者
Dodart, JC
Mathis, C
Bales, KR
Paul, MS
Ungerer, A
机构
[1] Univ Strasbourg 1, CNRS, URA 1295, Lab Ethol & Neurobiol, F-67000 Strasbourg, France
[2] Lilly Res Labs, Indianapolis, IN USA
关键词
Alzheimer; beta-amyloid precursor protein; apolipoprotein E; object recognition; memory; transgenic mice;
D O I
10.1097/00001756-200002280-00034
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Both the beta-amyloid precursor protein (APP) and the apoliprotein E (apoE) genes are involved in the pathogenesis of Alzheimer's disease (AD). We previously showed that mice over-expressing a human mutated form of APP (APP(V717F)) display age-dependent recognition memory deficits associated with the progression of amyloid deposition. Here, we asked whether 10- to 12-month-old APP(V717F) mice lacking the apoE gene, which do not present obvious amyloid deposition, differ from APP(V717F) mice in the object recognition task. The recognition performance is decreased in both transgenic mouse groups compared to control groups.;Moreover, some behavioral disturbances displayed by APP mice lacking apoE are even more pronounced than those of APP mice expressing apoE. Our results suggest that the recognition memory deficits are related to high levels of soluble A beta rather than to amyloid deposits. NeuroReport 11:603-607 (C) 2000 Lippincott Williams & Wilkins.
引用
收藏
页码:603 / 607
页数:5
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