A potential role for zinc alterations in the pathogenesis of Alzheimer's disease

被引：29

作者：

Lyubartseva, Ganna ^{[1
]}

Lovell, Mark A. ^{[2
,3
]}

机构：

[1] So Arkansas Univ, Dept Chem & Phys, Magnolia, AR 71753 USA

[2] Univ Kentucky, Dept Chem, Lexington, KY 40506 USA

[3] Univ Kentucky, Sanders Brown Ctr Aging, Alzheimers Dis Ctr, Lexington, KY 40536 USA

来源：

BIOFACTORS | 2012年 / 38卷 / 02期

关键词：

Alzheimer's disease; amyloid beta peptide; preclinical Alzheimer's disease; zinc; zinc transporter proteins; mild clinical impairment; MILD COGNITIVE IMPAIRMENT; AMYLOID-BETA PEPTIDE; TARGETING A-BETA; CEREBROSPINAL-FLUID; OXIDATIVE STRESS; SERUM ZINC; FUNCTIONAL-CHARACTERIZATION; CONFERS RESISTANCE; LINGUISTIC ABILITY; CORTICAL-NEURONS;

D O I：

10.1002/biof.199

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：

Alzheimer's disease (AD), one of the major causes of disability and mortality in Western societies, is a progressive age-related neurodegenerative disorder. Increasing evidence suggests that the etiology of AD may involve disruptions of zinc (Zn) homeostasis. This review discusses current evidence supporting a potential role of Zn and zinc transporters (ZnTs) in processing of the amyloid beta protein precursor (APP) and amyloid beta (A beta) peptide generation and aggregation.

引用

页码：98 / 106

页数：9

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