Roles of amyloid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment

Authors

D. Allan Butterfield
Tanea T. Reed, Eastern Kentucky UniversityFollow
Shelley F. Newman
Rukhsana Sultana

Author ORCID Identifier

Tanea Reedhttps://orcid.org/0000-0003-2642-3100

Department

Chemistry

Document Type

Article

Publication Date

9-1-2007

Abstract

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 Aβ(1-42) are discussed.

Recommended Citation

Butterfield, D. Allan; Reed, Tanea T.; Newman, Shelley F.; and Sultana, Rukhsana, "Roles of amyloid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment" (2007). EKU Faculty and Staff Scholarship. 642.
https://encompass.eku.edu/fs_research/642

Journal Title

Free Radical Biology and Medicine