Comparative characterization of 5XFAD and hAbetaSAA mouse models of familial AD

The failure of most clinical Alzheimer’s disease (AD) trials has been partially attributed to the lack of translatability of current AD mouse models to human patients. A recently developed model of familial AD (fAD), expressing Swedish, Arctic and Austrian mutations in App (hAbetaSAA), has been shown to be a useful amyloidogenic model which recapitulates many aspects of human AD, including plaque distribution and microglial transcriptional changes. Our aim is to further characterize the hAbetaSAA model and compare it to the widely used 5xFAD transgenic model.