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International Journal of Alzheimer’s Disease
Volume 2011 (2011), Article ID 971021, 10 pages
Review Article

The Role of Zinc in Alzheimer's Disease

Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Clarendon Way, Leeds LS2 9JT, UK

Received 14 September 2010; Accepted 9 November 2010

Academic Editor: Anthony R. White

Copyright © 2011 Nicole T. Watt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Zinc, the most abundant trace metal in the brain, has numerous functions, both in health and in disease. Zinc is released into the synaptic cleft of glutamatergic neurons alongside glutamate from where it interacts and modulates NMDA and AMPA receptors. In addition, zinc has multifactorial functions in Alzheimer's disease (AD). Zinc is critical in the enzymatic nonamyloidogenic processing of the amyloid precursor protein (APP) and in the enzymatic degradation of the amyloid-β (Aβ) peptide. Zinc binds to Aβ promoting its aggregation into neurotoxic species, and disruption of zinc homeostasis in the brain results in synaptic and memory deficits. Thus, zinc dyshomeostasis may have a critical role to play in the pathogenesis of AD, and the chelation of zinc is a potential therapeutic approach.