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Issue title: The Multifaceted Aspects of Alzheimer's Disease: From Social to Molecular Problems
Guest editors: Patrizia Mecocci
Article type: Research Article
Authors: Butterfield, D. Allana; b; c; * | Sultana, Rukhsanaa; b
Affiliations: [a] Department of Chemistry, University of Kentucky, Lexington, KY, USA | [b] Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA | [c] Center of Membrane Sciences, University of Kentucky, Lexington, KY, USA | Section of Gerontology and Geriatrics, Department of Clinical and Experimental Medicine, University of Perugia, Italy
Correspondence: [*] Corresponding author: Prof. D. Allan Butterfield, Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA. Tel.: +1 859 257 3184; Fax: +1 859 257 5876; E-mail: [email protected].
Abstract: Alzheimer disease is a common age-related neurodegenerative disease characterized pathologically by senile plaques, neurofibrillary tangles, synaptic disruption, and progressive neuronal deficits. The senile plaques contain amyloid-β (1–42) and amyloid-β (1–40), that has been shown by a number of laboratories to induce oxidative stress and as well as neurodegeneration, although the exact mechanisms remained to be defined. Our laboratory showed an increased oxidative stress in AD and MCI brain as indexed by protein oxidation and lipid peroxidation. In the present review, we summarize our finding of oxidatively modified proteins using a redox proteomics approach in AD and MCI brain to investigate the mechanism that may be involved in MCI and AD pathogenesis and discuss our findings in terms of AD progression and pathogenesis.
Keywords: Alzheimer's disease, mild cognitive impairment, oxidative stress, amyloid, redox proteomics
DOI: 10.3233/JAD-2007-12107
Journal: Journal of Alzheimer's Disease, vol. 12, no. 1, pp. 61-72, 2007
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