The missing link in the amyloid cascade of Alzheimer's disease - Metal ions

被引：71

作者：

Tiiman, Ann ^{[1
]}

Palumaa, Peep ^{[1
]}

Tougu, Vello ^{[1
]}

机构：

[1] Tallinn Univ Technol, Dept Gene Technol, EE-12618 Tallinn, Estonia

来源：

NEUROCHEMISTRY INTERNATIONAL | 2013年 / 62卷 / 04期

关键词：

Alzheimer's disease; Amyloid beta; Metal ions; A-BETA PEPTIDE; PRECURSOR PROTEIN APP; ZINC-BINDING SITE; E TYPE-4 ALLELE; APOLIPOPROTEIN-E; OXIDATIVE STRESS; TRANSGENIC MICE; PHYSIOLOGICAL FUNCTIONS; COGNITIVE IMPAIRMENT; CEREBROSPINAL-FLUID;

D O I：

10.1016/j.neuint.2013.01.023

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Progressive deposition of amyloid beta (A beta) peptides into amyloid plaques is the pathological hallmark of Alzheimer's disease (AD). The amyloid cascade hypothesis pins this deposition as the primary cause of the disease, but the mechanisms that causes this deposition remain elusive. An increasing amount of evidence shows that biometals Zn(II) and Cu(II) can interact with A beta, thus influencing the fibrillization and toxicity. This review focuses on the role of Zn(II) and Cu(II) in AD, and revisits the amyloid cascade hypothesis demonstrating the possible roles of Zn(II) and Cu(II) in the disease pathogenesis. (C) 2013 Elsevier Ltd. All rights reserved.

引用

页码：367 / 378

页数：12

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