AβPP accumulation and/or intraneuronal amyloid-β accumulation? The 3xTg-AD mouse model revisited

J Alzheimers Dis. 2012;28(4):897-904. doi: 10.3233/JAD-2011-111529.

Abstract

The triple-transgenic Alzheimer's disease (AD) mouse model, 3xTg-AD, played an important role in supporting the intraneuronal amyloid-β (Aβ) hypothesis in AD. However, recent evidence claims that the 3xTg-AD mice accumulate amyloid-β protein precursor (AβPP) instead of Aβ within neurons. In the present report, we re-investigated the 3xTg-AD mouse model and confirmed recent findings of age-dependent AβPP accumulations. In addition, intraneuronal Aβ was detected mainly in the neocortex using conformation-specific as well as antibodies directed against Aβ neo-epitopes. In contrast to previous work, however, only minor levels of intraneuronal Aβ were detected in the CA1 region of the hippocampus in aged 3xTg-AD mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology*
  • Amyloid beta-Peptides / analysis*
  • Amyloid beta-Protein Precursor / analysis*
  • Animals
  • Disease Models, Animal*
  • Mice
  • Mice, Transgenic
  • Neocortex / chemistry
  • Neocortex / pathology
  • Neurons / chemistry
  • Neurons / pathology*

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor