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 APP V717I (London) APP: Transgenic Alzheimer's Disease, Cerebral Amyloid Angiopathy Plaques start in the subiculum, spreading to the frontal cortex as dense and diffuse aggregates. Prominent amyloid deposits in brain vessels after 15 months. Microbleeds. Amyloid-associated inflammation. CSF Aβ42/Aβ40 ratio decreases from 15 months. Dystrophic neurites containing hyperphosphorylated tau, but no tangle pathology. From the age of 6 months, spatial and non-spatial orientation and memory deficits by Morris water maze. Impaired associative learning. Increased agitation/anxiety from 8 weeks. Reduced ambulation, especially with age. Hyperactivity and aggression. Yes Originally generated on FVB/N background; available at reMYND as C57BL/6xFVB/N Tg(Thy1-APPLon)2Vln/0 Increased mortality (72% by day 180). Increased incidence of seizures. Available through the KU Leuven Research and Development Office; the CRO reMYND offers research services with this line. Moechars et al., 1999
APP APP K670_M671delinsNL (Swedish) APP: Transgenic Alzheimer's Disease Numerous parenchymal Aβ plaques by 11-13 months with some vascular amyloid. Oxidative lipid damage, astrogliosis and microgliosis. No tangles or neuronal loss. Impaired spatial learning, working memory, and contextual fear conditioning reported at <6 months although other studies have reported normal cognition at this age with progressive impairment by >12 months. Yes B6;SJL Mixed Background B6;SJL-Tg(APPSWE)2576Kha Between 7 -12 weeks males become aggressive and begin to fight. Premature mortality: mortality of >20% anticipated, particularly in males. Taconic: Stock #1349 and Charles River.  The CROs PsychoGenics and QPS Austria offer research services with this line. Hsiao et al., 1996