Clearance of Alzheimer's Aβ peptide:: The many roads to perdition

被引：391

作者：

Tanzi, RE ^{[1
]}

Moir, RD

Wagner, SL

机构：

[1] Massachusetts Gen Hosp, Genet & Aging Res Unit, Massgen Inst Neurodegenerat Dis, Dept Neurol, Charlestown, MA 02129 USA

[2] Neurogenetics Inc, La Jolla, CA 92037 USA

来源：

NEURON | 2004年 / 43卷 / 05期

关键词：

D O I：

10.1016/j.neuron.2004.08.024

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The amyloid hypothesis of Alzheimer's disease (AD) maintains that the accumulation of the amyloid beta protein (Abeta) is a critical event in disease pathogenesis. A great deal of both academic and commercial research has focused on the mechanisms by which Abeta is generated. However, investigations into the mechanisms underlying Abeta clearance have blossomed over the last several years. This minireview will summarize pathways involved in the removal of cerebral Abeta, including enzymatic degradation and receptor-mediated efflux out of the brain.

引用

页码：605 / 608

页数：4

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