Single App knock-in mouse models of Alzheimer's disease

Nat Neurosci. 2014 May;17(5):661-3. doi: 10.1038/nn.3697. Epub 2014 Apr 13.

Abstract

Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP). These mice, however, suffer from artificial phenotypes because, in addition to amyloid β peptide (Aβ), they overproduce other APP fragments. We generated knock-in mice that harbor Swedish and Beyreuther/Iberian mutations with and without the Arctic mutation in the APP gene. The mice showed typical Aβ pathology, neuroinflammation and memory impairment in an age-dependent manner.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / genetics*
  • Analysis of Variance
  • Animals
  • Disease Models, Animal*
  • Enzyme-Linked Immunosorbent Assay
  • Gene Knock-In Techniques*
  • Humans
  • Maze Learning / physiology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mutation / genetics

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor