Endophilin I expression is increased in the brains of Alzheimer disease patients

Yimin Ren, Hong Wei Xu, Fleur Dieneke Davey, Margaret Alexandra Taylor, James Fortune Aiton, Peter John Coote, F Fang, J Yao, Doris Chen, JX Chen, SD Yan, Francis James Gunn-Moore

Research output: Contribution to journalArticlepeer-review

39 Citations (Scopus)

Abstract

Alzheimer patients have increased levels of both the 42 amyloid-beta-peptide(A beta) and the amyloid binding alcohol dehydrogenase (ABAD), which is an intracellular binding site for A beta. The overexpression of A beta and ABAD in transgenic mice has shown that the binding of A beta to ABAD results in amplified neuronal stress and impairment of learning and memory. From a proteomic analysis of the brains from these animals, we have identified for the first time that the protein endophilin I increases in Alzheimer diseased brain. The increase in endophilin I levels in neurons is linked to an increase in the activation of the stress kinase c-Jun N-terminal kinase with the subsequent death of the neurons. We also demonstrate in living animals that the expression level of endophilin I is an indicator for the interaction of ABAD and A beta as its expression levels return to normal if this interaction is perturbed. Therefore this identifies endophilin I as a new indicator of the progression of Alzheimer disease.

Original languageEnglish
Pages (from-to)5685-5691
Number of pages7
JournalJournal of Biological Chemistry
Volume283
Issue number9
DOIs
Publication statusPublished - 29 Feb 2008

Keywords

  • N-TERMINAL KINASE
  • AMYLOID-BETA-PEPTIDE
  • BINDING ALCOHOL-DEHYDROGENASE
  • ACTIVATED PROTEIN-KINASES
  • A-BETA
  • MITOCHONDRIAL DYSFUNCTION
  • NEURONAL APOPTOSIS
  • TRANSGENIC MICE
  • ABAD
  • STRESS

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