Apolipoprotein E alters the processing of the β-amyloid precursor protein in APPV717F transgenic mice

Jean Cosme Dodart, Kelly R. Bales, Edward M. Johnstone, Sheila P. Little, Steven M. Paul

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

We have recently reported a critical role for apolipoprotein E (apoE) in the process of amyloid deposition and neuritic plaque formation in APPV717F transgenic (Tg) mice, an animal model of Alzheimer's disease (AD). In the present study, we have investigated whether the presence or absence of apoE alters the processing of the amyloid precursor protein (APP) to various fragments, including the β-amyloid peptides (Aβ). Here we show that, in contrast to APPV717F Tg mice expressing apoE, APPV717F Tg mice deficient in apoE develop anti-Aβ immunoreactive multifocal aggregates, which contain the β-cleaved C-terminal fragments (β-CTFs) of APP. Tg mice deficient in apoE also display altered levels of mature full-length APP, increased amounts of β-CTFs, as well as elevated levels of Aβ1-40 and Aβ1-42 in an age- and region-dependent manner when compared to Tg mice expressing apoE. Taken together, these data support a role for apoE in APP processing in vivo.

Original languageEnglish
Pages (from-to)191-199
Number of pages9
JournalBrain Research
Volume955
Issue number1-2
DOIs
StatePublished - Nov 15 2002
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid precursor protein
  • Apolipoprotein E
  • Transgenic mouse

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