Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 43, Issue 5, Pages 658-677Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2007.05.037
Keywords
Alzheimer's disease; mild cognitive impairment; oxidative stress; amyloid beta-peptide; redox proteomics; free radicals
Funding
- NIA NIH HHS [P01 AG005119-110001, P01 AG010836-120011, P01 AG010836-130011, P01 AG005119-140001, P01 AG005119, P01 AG005119-130001, P01 AG005119-13S10001, AG-05119, AG-10836, P01 AG005119-150006, P01 AG010836-110011, P01 AG005119-120001, P01 AG010836-140011, P01 AG010836, P01 AG005119-12S20001] Funding Source: Medline
- NATIONAL INSTITUTE ON AGING [P01AG010836, P01AG005119] Funding Source: NIH RePORTER
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Oxidative stress has been implicated to play a crucial role in the pathogenesis of a number of diseases, including neurodegenerative disorders, cancer, and ischemia, just to name a few. Alzheimer disease (AD) is an age-related neurodegenerative disorder that is recognized as the most common form of dementia. AD is histopathologically characterized by the presence of extracellular amyloid plaques, intracellular neurofibrillary tangles, the presence of oligomers of amyloid beta-peptide (A beta), and synapse loss. In this review we discuss the role of A beta in the pathogenesis of AD and also the use of redox proteomics to identify oxidatively modified brain proteins in AD and mild cognitive impairment. In addition, redox proteomics studies in in vivo models of AD centered around human A beta(1-42) are discussed. (c) 2007 Elsevier Inc. All rights reserved.
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