Proteomic identification of proteins specifically oxidized in Caenorhabditis elegans expressing human Aβ(1-42): Implications for Alzheimer's disease

Debra Boyd-Kimball, H. Fai Poon, Bert C. Lynn, Jian Cai, William M. Pierce, Jon B. Klein, Jmil Ferguson, Christopher D. Link, D. Allan Butterfield

Research output: Contribution to journalArticlepeer-review

79 Scopus citations

Abstract

Protein oxidation has been shown to lead to loss of protein function, increased protein aggregation, decreased protein turnover, decreased membrane fluidity, altered cellular redox poteintial, loss of Ca2+ homeostaisis, and cell death. There is increasing evidence that protein oxidation is involved in the pathogenesis of Alzheimer's disease and amyloid beta-peptide (1-42) has been implicated as a mediator of oxidative stress in AD. However, the specific implications of the oxidation induced by Aβ(1-42) on the neurodegeneration evident in AD are unknown. In this study, we used proteomic techniques to identify specific targets of oxidation in transgenic Caenorhabditis elegans (C. elegans) expressing human Aβ(1-42). We identified 16 oxidized proteins involved in energy metabolism, proteasome function, and scavenging of oxidants that are more oxidized compared to control lines. These results are discussed with reference to Alzheimer's disease.

Original languageEnglish
Pages (from-to)1239-1249
Number of pages11
JournalNeurobiology of Aging
Volume27
Issue number9
DOIs
StatePublished - Sep 2006

Bibliographical note

Funding Information:
This work was supported in part by NIH grants to D.A.B. [AG-05119; AG-10836] and C.D.L [AG12423, AG21037]. We are indebted to Creg Darby for providing the XA1440 strain.

Keywords

  • Alzheimer's disease
  • Amyloid β-peptide
  • C. elegans
  • Protein oxidation
  • Proteomics

ASJC Scopus subject areas

  • General Neuroscience
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

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