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 β-peptide (Aβ), and synapse loss. In this review we discuss the role of Aβ 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 Aβ(1-42) are discussed.
|Number of pages||20|
|Journal||Free Radical Biology and Medicine|
|State||Published - Sep 1 2007|
Bibliographical noteFunding Information:
This work was supported in part by grants from the National Institutes of Health (AG-05119, AG-10836).
- Alzheimer's disease
- Amyloid β-peptide
- Free radicals
- Mild cognitive impairment
- Oxidative stress
- Redox proteomics
ASJC Scopus subject areas
- Physiology (medical)