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Zinc overload enhances APP cleavage and Aβ deposition in the Alzheimer mouse brain.

PloS one (2010-12-24)
Chun-Yan Wang, Tao Wang, Wei Zheng, Bao-Lu Zhao, Gorm Danscher, Yu-Hua Chen, Zhan-You Wang
ABSTRACT

Abnormal zinc homeostasis is involved in β-amyloid (Aβ) plaque formation and, therefore, the zinc load is a contributing factor in Alzheimer's disease (AD). However, the involvement of zinc in amyloid precursor protein (APP) processing and Aβ deposition has not been well established in AD animal models in vivo. In the present study, APP and presenilin 1 (PS1) double transgenic mice were treated with a high dose of zinc (20 mg/ml ZnSO4 in drinking water). This zinc treatment increased APP expression, enhanced amyloidogenic APP cleavage and Aβ deposition, and impaired spatial learning and memory in the transgenic mice. We further examined the effects of zinc overload on APP processing in SHSY-5Y cells overexpressing human APPsw. The zinc enhancement of APP expression and cleavage was further confirmed in vitro. The present data indicate that excess zinc exposure could be a risk factor for AD pathological processes, and alteration of zinc homeostasis is a potential strategy for the prevention and treatment of AD.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-Amyloid Precursor Protein, C-Terminal antibody produced in rabbit, IgG fraction of antiserum, buffered aqueous solution
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Monoclonal Anti-β-Amyloid antibody produced in mouse, clone BAM-10, ascites fluid
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Anti-BACE 1, N-Terminus (46-62) antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution
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Anti-ADAM 10 Antibody, CT, Chemicon®, from rabbit
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Anti-Presenilin-1 Antibody, NT, clone hPS1-NT, culture supernatant, clone hPS1-NT, Chemicon®
Sigma-Aldrich
Anti-Amyloid Precursor Protein Antibody, CT, serum, Chemicon®

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