Copper in Alzheimer's disease: too much or too little?

Joseph F. Quinn; Susanne Crane; Christopher Harris; Teri L. Wadsworth

doi:10.1586/ern.09.27

Copper in Alzheimer's disease: too much or too little?

Joseph F. Quinn, Susanne Crane, Christopher Harris, Teri L. Wadsworth

Neurology

Research output: Contribution to journal › Review article › peer-review

32 Scopus citations

Abstract

A considerable amount of literature has accrued examining the role of copper in the pathogenesis of Alzheimer's disease. Remarkably, there is in vitro and animal data to support both copper toxicity and copper deficiency as relevant mechanisms in Alzheimer's disease. These data have prompted preliminary clinical trials of both copper complexing therAβy and copper supplementation therAβy, which have yielded mixed results. The preclinical and clinical studies are discussed here in an effort to determine how to move forward with rational clinical trials focused on copper modulation.

Original language	English (US)
Pages (from-to)	631-637
Number of pages	7
Journal	Expert Review of Neurotherapeutics
Volume	9
Issue number	5
DOIs	https://doi.org/10.1586/ern.09.27
State	Published - May 2009

Keywords

Alzheimer's disease
Animal model
Chelation
Clinical trial
Copper
Oxidative damage

ASJC Scopus subject areas

Neuroscience(all)
Clinical Neurology
Pharmacology (medical)

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10.1586/ern.09.27

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title = "Copper in Alzheimer's disease: too much or too little?",

abstract = "A considerable amount of literature has accrued examining the role of copper in the pathogenesis of Alzheimer's disease. Remarkably, there is in vitro and animal data to support both copper toxicity and copper deficiency as relevant mechanisms in Alzheimer's disease. These data have prompted preliminary clinical trials of both copper complexing therAβy and copper supplementation therAβy, which have yielded mixed results. The preclinical and clinical studies are discussed here in an effort to determine how to move forward with rational clinical trials focused on copper modulation.",

keywords = "Alzheimer's disease, Animal model, Chelation, Clinical trial, Copper, Oxidative damage",

author = "Quinn, {Joseph F.} and Susanne Crane and Christopher Harris and Wadsworth, {Teri L.}",

note = "Funding Information: This work was supported by NIA (R21AG027445A) and the Department of Veteran{\textquoteright}s Affairs. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.",

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AU - Quinn, Joseph F.

AU - Crane, Susanne

AU - Harris, Christopher

AU - Wadsworth, Teri L.

N1 - Funding Information: This work was supported by NIA (R21AG027445A) and the Department of Veteran’s Affairs. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

PY - 2009/5

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N2 - A considerable amount of literature has accrued examining the role of copper in the pathogenesis of Alzheimer's disease. Remarkably, there is in vitro and animal data to support both copper toxicity and copper deficiency as relevant mechanisms in Alzheimer's disease. These data have prompted preliminary clinical trials of both copper complexing therAβy and copper supplementation therAβy, which have yielded mixed results. The preclinical and clinical studies are discussed here in an effort to determine how to move forward with rational clinical trials focused on copper modulation.

AB - A considerable amount of literature has accrued examining the role of copper in the pathogenesis of Alzheimer's disease. Remarkably, there is in vitro and animal data to support both copper toxicity and copper deficiency as relevant mechanisms in Alzheimer's disease. These data have prompted preliminary clinical trials of both copper complexing therAβy and copper supplementation therAβy, which have yielded mixed results. The preclinical and clinical studies are discussed here in an effort to determine how to move forward with rational clinical trials focused on copper modulation.

KW - Alzheimer's disease

KW - Animal model

KW - Chelation

KW - Clinical trial

KW - Copper

KW - Oxidative damage

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Copper in Alzheimer's disease: too much or too little?

Abstract

Keywords

ASJC Scopus subject areas

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