Research Models

Commonly Used Mouse Models

Name Genes Mutations Modification Disease Neuropathology Behavior/Cognition Visualization Promoter/Regulatory Elements Genetic Background Strain Name Other Phenotypes Availability Primary Paper
APP, PSEN1 APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V APP: Transgenic; PSEN1: Transgenic Alzheimer's Disease Amyloid pathology starting at 2 months, including amyloid plaques. Accumulation of intraneuronal Aβ before amyloid deposition. Gliosis and synapse degeneration. Neuron loss in cortical layer 5 and subiculum. No neurofibrillary tangles. Age-dependent memory deficits including spatial memory, stress-related memory, and memory stablization. Motor phenotype. Yes C57BL/6 x SJL B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax The Jackson Lab; available through the JAX MMRRC Stock# 034840; Live. Oakley et al., 2006
APP APP K670_M671delinsNL (Swedish), APP I716F (Iberian), APP E693G (Arctic) APP: Knock-In Alzheimer's Disease Aggressive amyloidosis with deposition in the cortex beginning at 2 months and approaching saturation by 7 months. Aβ deposition in heterozygous mice at 4 months. Subcortical amyloidosis. Exacerbated microgliosis and astrocytosis compared to APPNL-F mice. Reduced synaptophysin and PSD-95 indicative of synaptic loss. No tangle pathology or neurodegeneration. Memory impairment by 6 months as measured by the Y maze. Yes C57BL/6 Apptm3.1Tcs/Apptm3.1Tcs No overexpression of APP. Wild-type levels of AICD. Available through Takaomi Saido Saito et al., 2014