Behavioral deficits in APP(V717F) transgenic mice deficient for the apolipoprotein E gene

J. C. Dodart, C. Mathis, K. R. Bales, S. M. Paul, A. Ungerer

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

Both the β-amyloid precursor protein (APP) and the apolipoprotein E (apoE) genes are involved in the pathogenesis of Alzheimer's disease (AD). We previously showed that mice over-expressing a human mutated form of APP (APP(V717F)) display age-dependent recognition memory deficits associated with the progression of amyloid deposition. Here, we asked whether 10- to 12- month-old APP(V717F) mice lacking the apoE gene, which do not present obvious amyloid deposition, differ from APP(V717F) mice in the object recognition task. The recognition performance is decreased in both transgenic mouse groups compared to control groups. Moreover, some behavioral disturbances displayed by APP mice lacking apoE are even more pronounced than those of APP mice expressing apoE. Our results suggest that the recognition memory deficits are related to high levels of soluble Aβ rather than to amyloid deposits. (C) 2000 Lippincott Williams and Wilkins.

Original languageEnglish
Pages (from-to)603-607
Number of pages5
JournalNeuroReport
Volume11
Issue number3
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

Keywords

  • Alzheimer
  • Apolipoprotein E
  • Memory
  • Object recognition
  • Transgenic mice
  • β-Amyloid precursor protein

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