The role of zinc in Alzheimer's disease

Nigel M. Hooper; Nicole T. Watt; Isobel J. Whitehouse

doi:10.4061/2011/971021

The role of zinc in Alzheimer's disease

Nigel M. Hooper, Nicole T. Watt, Isobel J. Whitehouse

Research output: Contribution to journal › Article › peer-review

Abstract

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. Copyright © 2011 Nicole T. Watt et al.

Original language	English
Article number	971021
Journal	International Journal of Alzheimer's Disease
DOIs	https://doi.org/10.4061/2011/971021
Publication status	Published - 2011

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http://www.ncbi.nlm.nih.gov/pubmed/21197404

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title = "The role of zinc in Alzheimer's disease",

abstract = "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. Copyright {\textcopyright} 2011 Nicole T. Watt et al.",

author = "Hooper, {Nigel M.} and Watt, {Nicole T.} and Whitehouse, {Isobel J.}",

note = "Watt, Nicole T Whitehouse, Isobel J Hooper, Nigel M England Int J Alzheimers Dis. 2010 Dec 20;2011:971021.",

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AU - Whitehouse, Isobel J.

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AB - 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. Copyright © 2011 Nicole T. Watt et al.

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DO - 10.4061/2011/971021

M3 - Article

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JO - International Journal of Alzheimer's Disease

JF - International Journal of Alzheimer's Disease

M1 - 971021

ER -

The role of zinc in Alzheimer's disease

Abstract

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