Amyloid-β and tau - a toxic pas de deux in Alzheimer's disease

被引：1090

作者：

Ittner, Lars M. ^{[1
]}

Goetz, Juergen ^{[1
]}

机构：

[1] Univ Sydney, Alzheimers & Parkinsons Dis Lab, Brain & Mind Res Inst, Camperdown, NSW 2050, Australia

来源：

NATURE REVIEWS NEUROSCIENCE | 2011年 / 12卷 / 02期

基金：

英国医学研究理事会; 澳大利亚研究理事会;

关键词：

A-BETA; PROTEIN-TAU; SYNAPTIC PLASTICITY; ANIMAL-MODELS; PRION PROTEIN; MOUSE MODEL; PHOSPHORYLATION; DEGENERATION; NEURODEGENERATION; LOCALIZATION;

D O I：

10.1038/nrn2967

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Amyloid-beta and tau are the two hallmark proteins in Alzheimer's disease. Although both amyloid-beta and tau have been extensively studied individually with regard to their separate modes of toxicity, more recently new light has been shed on their possible interactions and synergistic effects in Alzheimer's disease. Here, we review novel findings that have shifted our understanding of the role of tau in the pathogenesis of Alzheimer's disease towards being a crucial partner of amyloid-beta. As we gain a deeper understanding of the different cellular functions of tau, the focus shifts from the axon, where tau has a principal role as a microtubule-associated protein, to the dendrite, where it mediates amyloid-beta toxicity.

引用

页码：67 / 72

页数：6

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