Interaction of amyloid binding alcohol dehydrogenase/Aβ mediates up-regulation of peroxiredoxin II in the brains of Alzheimer's disease patients and a transgenic Alzheimer's disease mouse model

Jun Yao, Margaret Taylor, Fleur Davey, Yimin Ren, Jim Aiton, Peter Coote, Fang Fang, John Xi Chen, Shi Du Yan, Frank J. Gunn-Moore

Research output: Contribution to journalArticlepeer-review

70 Citations (Scopus)

Abstract

Alzheimer's patients have increased levels of both the 42 beta amyloid-beta-peptide (A beta) and amyloid binding alcohol dehydrogenase (ABAD) which is an intraceflular binding site for A beta. The over-expression of A beta and ABAD in transgenic mice has shown that the binding of AD to ABAD results in exaggerating neuronal stress and impairment of learning and memory. From a proteomic analysis of the brains from these animals we identified that peroxiredoxin II levels increase in Alzheimer's diseased brain. This increase in peroxiredoxin II levels protects neurons against A beta induced toxicity. We also demonstrate, for the first time in living animals, that the expression level of peroxidredoxin II is an indicator for the interaction of ABAD and AD as its expression levels return to normal if this interaction is perturbed. Therefore this indicates the possibility of reversing changes observed in Alzheimer's disease and that the A beta-ABAD interaction is a suitable drug target. (c) 2007 Elsevier Inc. All rights reserved.

Original languageEnglish
Pages (from-to)377-382
Number of pages6
JournalMolecular and Cellular Neuroscience
Volume35
Issue number2
DOIs
Publication statusPublished - Jun 2007

Keywords

  • proteomics
  • neuronal stress
  • ABAD
  • amyloid
  • Alzheimer's disease
  • A-BETA
  • MITOCHONDRIAL DYSFUNCTION
  • PROTEIN TRANSDUCTION
  • PEPTIDE
  • CELLS
  • EXPRESSION
  • MECHANISM
  • SUBTYPES
  • PATHWAY

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