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Issue 9, 2016
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Metallo-pathways to Alzheimer's disease: lessons from genetic disorders of copper trafficking

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Abstract

Copper is an essential metal ion that provides catalytic function to numerous enzymes and also regulates neurotransmission and intracellular signaling. Conversely, a deficiency or excess of copper can cause chronic disease in humans. Menkes and Wilson disease are two rare heritable disorders of copper transport that are characterized by copper deficiency and copper overload, respectively. Changes to copper status are also a common feature of several neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD) and Amyotrophic lateral sclerosis (ALS). In the case of AD, which is characterized by brain copper depletion, changes in the distribution of copper has been linked with various aspects of the disease process; protein aggregation, defective protein degradation, oxidative stress, inflammation and mitochondrial dysfunction. Although AD is a multifactorial disease that is likely caused by a breakdown in multiple cellular pathways, copper and other metal ions such as iron and zinc play a central role in many of these cellular processes. Pioneering work by researchers who have studied relatively rare copper transport diseases has shed light on potential metal ion related disease mechanisms in other forms of neurodegeneration such as AD.

Graphical abstract: Metallo-pathways to Alzheimer's disease: lessons from genetic disorders of copper trafficking

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Publication details

The article was received on 08 Apr 2016, accepted on 29 Jun 2016 and first published on 29 Jun 2016


Article type: Minireview
DOI: 10.1039/C6MT00095A
Metallomics, 2016,8, 831-839

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    Metallo-pathways to Alzheimer's disease: lessons from genetic disorders of copper trafficking

    M. A. Greenough, A. Ramírez Munoz, A. I. Bush and C. M. Opazo, Metallomics, 2016, 8, 831
    DOI: 10.1039/C6MT00095A

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