Cited by 98Alzheimer's disease research and treatmentsRedox biology and oxidative stressDementia and Cognitive Impairment Research

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

Boyd-Kimball, Debra, Poon, H. Fai, Lynn, Bert C., Cai, Jian, Pierce Jr., William M., Klein, Jon B., Ferguson, Jmil, Link, Christopher D. +1 more·2006·Neurobiology of Aging

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 Abeta(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 Abeta(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.

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Crossref · 10.1016/j.neurobiolaging.2005.07.001

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  • MDH is oxidatively modified by HNE in early AD inferior parietal lobule and its carbonylation is induced by Aβ in vitro and in vivo.

    “MDH is oxidatively modified by HNE in early AD inferior parietal lobule (IPL) [55] and its carbonylation is induced by Aβ in vitro and in vivo [63,65,66].”

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Authors
Boyd-Kimball, D., Poon, H. F., Lynn, B. C., Cai, J., Pierce Jr., W. M., Klein, J. B., Ferguson, J., Link, C. D., & Butterfield, D. A.
Affiliations
  • University of Kentucky (US)
  • University of Louisville (US)
  • University of Colorado Boulder (US)
Corresponding author
Butterfield, D. Allan
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2006-09
Volume
27
Issue
9
Pages
1239-1249
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2167590630
Cited by
98
References
58
Citations by year
2024: 2 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 5 · 2014: 4 · 2013: 8 · 2012: 7
FWCI
5.79
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (P01AG010836, P01AG005119, AG21037, R01AG021037, AG 10836, AG12423, AG0 5119, R01AG012423)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
protein oxidation, amyloid-beta, Alzheimer's disease, Caenorhabditis elegans, transgenic Caenorhabditis elegans, oxidative stress, oxidized proteins, energy metabolism, proteasome function, antioxidant scavenging, neurodegeneration, protein aggregation
MeSH terms
Analysis of Variance, Animals, Humans, Oxidation-Reduction, Peptide Fragments, Mass Spectrometry, Blotting, Western, Electrophoresis, Gel, Two-Dimensional, Gene Expression, Amyloid beta-Peptides, Caenorhabditis elegans, Oxidative Stress, Sequence Analysis, Protein, Caenorhabditis elegans Proteins, Animals, Genetically Modified, Proteomics

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