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Issue 3, 2011
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Role of metal dyshomeostasis in Alzheimer's disease

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Abstract

Despite serving a crucial purpose in neurobiological function, transition metals play a sinister part in the aging brain, where the abnormal accumulation and distribution of reactive iron, copper, and zinc elicit oxidative stress and macromolecular damage that impedes cellular function. Alzheimer's disease (AD), an age-related neurodegenerative condition, presents marked accumulations of oxidative stress-induced damage, and increasing evidence points to aberrant transition metal homeostasis as a critical factor in its pathogenesis. Amyloid-β oligomerization and fibrillation, considered by many to be the precipitating factor underlying AD onset and development, is also induced by abnormal transition metal activity. We here elaborate on the roles of iron, copper, and zinc in AD and describe the therapeutic implications they present.

Graphical abstract: Role of metal dyshomeostasis in Alzheimer's disease

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Publication details

The article was received on 10 Nov 2010, accepted on 26 Jan 2011 and first published on 07 Feb 2011


Article type: Minireview
DOI: 10.1039/C0MT00074D
Citation: Metallomics, 2011,3, 267-270
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    Role of metal dyshomeostasis in Alzheimer's disease

    D. J. Bonda, H. Lee, J. A. Blair, X. Zhu, G. Perry and M. A. Smith, Metallomics, 2011, 3, 267
    DOI: 10.1039/C0MT00074D

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