Expression of APP in transgenic mice: a Comparison of neuron-specific promoters
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2019, Epilepsy and BehaviorBrainwide distribution and variance of amyloid-beta deposits in tg-ArcSwe mice
2014, Neurobiology of AgingAPP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)
2012, Neuroscience and Biobehavioral ReviewsCitation Excerpt :APP/DU/Thy1 and APP/FL/Thy1 mice with Dutch (E693Q) and Flemish (A692G) mutations, respectively, each driven by the murine Thy1 promoter, have cerebral amyloid angiopathy with elevated C-terminal fragments in parenchymal regions but without Aβ plaques (Kumar-Singh et al., 2000), thus serving as animal models of cerebral amyloid angiopathy caused by such mutations. A second APP/DU/THY1 model with the human THY1 promoter also has cerebral amyloid angiopathy without Aβ plaques (Andrä et al., 1996; Gandy et al., 2010). Five models characterized by combined Swedish/Indiana mutations are available.
β-amyloid peptide variants in brains and cerebrospinal fluid from amyloid precursor protein (APP) transgenic mice: Comparison with human Alzheimer amyloid
2011, Journal of Biological ChemistryCitation Excerpt :The APP23 mouse line (18) represents one out of several well established transgenic mouse models that display key features of the amyloid pathology observed in patients with Alzheimer disease (for review, see Ref. 19). Human APP751 carrying the Swedish double mutation (K670N/M671L) is overexpressed in APP23 mice under control of the murine Thy-1 promoter, which drives neuron-specific expression (20). At ∼6 months of age, the first amyloid deposits are observed in heterozygous animals (18).