Alzheimer's Pathology in Transgenic Mice

APPswe/PS1dE9 transgenic (APP/PS1) or age- and sex-matched C57BL/6J wild-type (WT) littermates were bred and aged at Brigham and Women’s Hospital (BWH) (Boston, MA, USA). APPswe/PS1dE9 mice have the Swedish APP^K594N/M595L human transgene as well as the PS1dE9 human transgene, both of which are under a mouse prion promotor [59 (link)]. APPswe/PS1dE9 mice exhibit AD pathology including extracellular amyloid deposits in the prefrontal cortex and hippocampus by 5–6 months of age, Aβ plaque deposition, microhemorrhages, gliosis, and cognitive deficits by 7–8 months of age [60 (link),61 (link),62 (link)]. Mice were transferred to Brookhaven National Laboratory (BNL) in Upton, NY, USA irradiated at 4 months of age, and returned to BWH where they underwent quarantine before being moved back into the mouse colony. Mice underwent behavioral testing at 11 months of age and were euthanized by CO₂ exposure at 12 months of age. At both BWH and BNL, mice were housed at a constant temperature on a 12 h light/dark cycle and had ad libitum access to food (PicoLab Rodent Diet #5053) and water. All animal use was approved by the Harvard Medical School Office for Research Subject Protection—Harvard Medical Area Standing Committee on Animals and the Brookhaven National Laboratory Institutional Animal Care and Use Committee.