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Article type: Review Article
Authors: Lovell, Mark A.; *
Affiliations: Department of Chemistry and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA
Correspondence: [*] Corresponding author: Mark A. Lovell, 135 Sanders-Brown Building, 800 S. Limestone St., Lexington, KY 40536, USA. E-mail: [email protected].
Abstract: Although multiple studies have suggested a role for alterations of zinc (Zn) and zinc transport (ZnT) proteins in the pathogenesis of Alzheimer's disease, the exact role of this essential trace element in the progression of the disease remains unclear. The following review discusses the normal role of Zn and ZnT proteins in brain and the potential effects of their alteration in the pathogenesis of Alzheimer's disease, particularly in the processing of the amyloid-β protein precursor and amyloid-β peptide generation and aggregation.
Keywords: Amyloid-β, early Alzheimer's disease, mild cognitive impairment, zinc, zinc transport proteins
DOI: 10.3233/JAD-2009-0992
Journal: Journal of Alzheimer's Disease, vol. 16, no. 3, pp. 471-483, 2009
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