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 therapy and copper supplementation therapy, 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

Financial & competing interests disclosure

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.

No writing assistance was utilized in the production of this manuscript.