Transgenic models of Alzheimer's disease: Learning from animals

被引：151

作者：

Spires T.L. ^{[1
]}

Hyman B.T. ^{[1
]}

机构：

[1] Massachusetts General Hospital, Department of Neurology, Alzheimer's Disease Research Laboratory, Charlestown, MA 02129

来源：

NeuroRX | 2005年 / 2卷 / 3期

基金：

美国国家卫生研究院;

关键词：

Amyloid; Neurofibrillary tangle; Senile plaque; Tau; Transgenic;

D O I：

10.1602/neurorx.2.3.423

中图分类号：

学科分类号：

摘要：

As the scope of the problem of Alzheimer's disease (AD) grows due to an aging population, research into the devastating condition has taken on added urgency. Rare inherited forms of AD provide insight into the molecular pathways leading to degeneration and have made possible the development of transgenic animal models. Several of these models are based on the overexpression of amyloid precursor protein (APP), presenilins, or tau to cause production and accumulation of amyloid-β into plaques or hyperphosphorylated tau into neurofibrillary tangles. Producing these characteristic neuropathological lesions in animals causes progressive neurodegeneration and in some cases similar behavioral disruptions to those seen in AD patients. Knockout models of proteins involved in AD have also been generated to explore the native functions of these genes and examine whether pathogenesis is due to loss of function or toxic gain of function in these systems. Although none of the transgenic lines models the human condition exactly, the ability to study similar pathological processes in living animals have provided numerous insights into disease mechanisms and opportunities to test therapeutic agents. This chapter reviews animal models of AD and their contributions to developing therapeutic approaches for AD. © The American Society for Experimental NeuroTherapeutics, Inc.

引用

页码：423 / 437

页数：14

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