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

D. Allan Butterfield, Tanea Reed, Shelley F. Newman, Rukhsana Sultana

Research output: Contribution to journalReview articlepeer-review

488 Scopus citations

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 human Aβ(1-42) are discussed.

Original languageEnglish
Pages (from-to)658-677
Number of pages20
JournalFree Radical Biology and Medicine
Volume43
Issue number5
DOIs
StatePublished - Sep 1 2007

Bibliographical note

Funding Information:
This work was supported in part by grants from the National Institutes of Health (AG-05119, AG-10836).

Keywords

  • Alzheimer's disease
  • Amyloid β-peptide
  • Free radicals
  • Mild cognitive impairment
  • Oxidative stress
  • Redox proteomics

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

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