hAPP tg Mice
hAPP transgenic mice over-express human APP751SL under the control of the murine Thy-1 promoter. The animals contain the same gene construct as described in Rockenstein et al. (2001). This human APP with London (717) and Swedish (670/671) mutations is expressed in high levels, resulting in an age-dependent increase of ß-amyloid1-40 and ß-amyloid1-42, the pathologically relevant forms of amyloid protein. The mice develop plaques consisting of amyloid depositions in early age, starting at 3 – 6 months in the frontal cortex. Severity of the brain pathology correlates with increasing age and behavioral deficits.
JSW hAPP tg mice are a suitable model to study the influence of drugs on amyloid production, sequestration and deposition.
