Amyloid β-Peptide [1-42]-Associated Free Radical-Induced Oxidative Stress And Neurodegeneration in Alzheimer's Disease Brain: Mechanisms and Consequences

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Abstract:

In addition to synapse loss, neurofibrillary tangles, and neurodegeneration, oxidative stress and amyloid β-peptide [Aβ] deposition are hallmarks of Alzheimer's disease [AD] brain. Our laboratory coupled these two characteristics of AD into a comprehensive model to account for the synapse loss and neurodegeneration in AD brain. This model combines much of the extant studies on AD and is based on oxidative stress associated with amyloid β-peptide. This review presents evidence in support of this model and provides insight into the molecular basis of this devastating dementing disorder.

Keywords: amyloid b-peptide; free radicals; lipid peroxidation; neurodegeneration; oxidative stress; protein oxidation; proteomics

Document Type: Review Article

DOI: http://dx.doi.org/10.2174/0929867033456422

Affiliations: Department of Chemistry; Center of Membrane Sciences; and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506 USA.

Publication date: December 1, 2003

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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