May 15, 2013

Normal cognition in transgenic BRI2-Aβ mice

Molecular Neurodegeneration
Jungsu KimChristopher Janus

Abstract

Recent research in Alzheimer's disease (AD) field has been focused on the potential role of the amyloid-β protein that is derived from the transmembrane amyloid precursor protein (APP) in directly mediating cognitive impairment in AD. Transgenic mouse models overexpressing APP develop robust AD-like amyloid pathology in the brain and show various levels of cognitive decline. In the present study, we examined the cognition of the BRI2-Aβ transgenic mouse model in which secreted extracellular Aβ1-40, Aβ1-42 or both Aβ1-40/Aβ1-42 peptides are generated from the BRI-Aβ fusion proteins encoded by the transgenes. BRI2-Aβ mice produce high levels of Aβ peptides and BRI2-Aβ1-42 mice develop amyloid pathology that is similar to the pathology observed in mutant human APP transgenic models. Using established behavioral tests that reveal deficits in APP transgenic models, BRI2-Aβ1-42 mice showed completely intact cognitive performance at ages both pre and post amyloid plaque formation. BRI2-Aβ mice producing Aβ1-40 or both peptides were also cognitively intact. These data indicate that high levels of Aβ1-40 or Aβ1-42, or both produced in the absence of APP overexpression do not reproduce memory deficits observed in APP transgenic mouse mod...Continue Reading

  • References60
  • Citations22

References

  • References60
  • Citations22

Citations

Mentioned in this Paper

Familial Alzheimer Disease (FAD)
Derivatives
APP protein, human
Extracellular
Amyloid beta-protein (1-40)
Amyloid Beta Precursor Protein Measurement
Brain
Plaque, Amyloid
Immunocytochemistry
Integral to Membrane

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