Does my mouse have Alzheimer's disease?

被引:95
作者
Dodart, JC [1 ]
Mathis, C
Bales, KR
Paul, SM
机构
[1] Eli Lilly & Co, Neurosci Discovery Res, Indianapolis, IN 46285 USA
[2] ULP, IFR Neurosci, CNRS, UMR 7521,Lab Neurosci Comportementales & Cognit, Strasbourg, France
关键词
A beta; Alzheimer's disease; amyloid; APP; behavior; learning and memory; neuropathology; transgenic mouse models;
D O I
10.1034/j.1601-183X.2002.10302.x
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Small animal models that manifest many of the characteristic neuropathological and behavioral features of Alzheimer's disease (AD) have been developed and have proven of great value for studying the pathogenesis of this disorder at the molecular, cellular and behavioral levels. The great progress made in our understanding of the genetic factors that either cause or contribute to the risk of developing AD has prompted many laboratories to create transgenic (tg) mice that overexpress specific genes which cause familial forms of the disease. Several of these tg mice display neuropathological and behavioral features of AD including amyloid beta-peptide (Abeta) and amyloid deposits, neuritic plaques, gliosis, synaptic alterations and signs of neurodegeneration as well as memory impairment. Despite these similarities, important differences in neuropathology and behavior between these tg mouse models and AD have also been observed, and to date no perfect animal model has emerged. Moreover, ascertaining which elements of the neuropathological and behavioral phenotype of these various strains of tg mice are relevant to that observed in AD continues to be a challenge. Here we provide a critical review of the AD-like neuropathology and behavioral phenotypes of several well-known and utilized tg mice that express human APP transgenes.
引用
收藏
页码:142 / 155
页数:14
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