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International Journal of Alzheimer’s Disease
Volume 2011, Article ID 370345, 5 pages
Review Article

Copper Modulation as a Therapy for Alzheimer's Disease?

1Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Autonomous University of Barcelona, Bellaterra, 08193 Barcelona, Spain
2Oxidation Biology Laboratory, The Mental Health Research Institute, Parkville, Vic 3052, Australia
3Synaptic Neurobiology Laboratory, The Mental Health Research Institute, Parkville, Vic 3052, Australia
4Department of Pathology, The University of Melbourne, Parkville, Vic 3010, Australia

Received 24 May 2011; Accepted 30 June 2011

Academic Editor: Rosanna Squitti

Copyright © 2011 Yasmina Manso 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.


The role of metals in the pathophysiology of Alzheimer's disease (AD) has gained considerable support in recent years, with both in vitro and in vivo data demonstrating that a mis-metabolism of metal ions, such as copper and zinc, may affect various cellular cascades that ultimately leads to the development and/or potentiation of AD. In this paper, we will provide an overview of the preclinical and clinical literature that specifically relates to attempts to affect the AD cascade by the modulation of brain copper levels. We will also detail our own novel animal data, where we treated APP/PS1 (7-8 months old) mice with either high copper (20 ppm in the drinking water), high cholesterol (2% supplement in the food) or a combination of both and then assessed β-amyloid (Aβ) burden (soluble and insoluble Aβ), APP levels and behavioural performance in the Morris water maze. These data support an interaction between copper/cholesterol and both Aβ and APP and further highlight the potential role of metal ion dyshomeostasis in AD.