29625 RESULTS
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RESEARCH MODELS Summary These double transgenic mice were generated in the mid-1990s by David Borchelt, Sangram Sisodia, and colleagues at Johns Hopkins. The mice were made by crossing two transgenic lines, one expressing human PSEN1 with the A246E mutation and another l
RESEARCH MODELS Summary These mice express human APP with the Swedish (K670N/M671L) and London (V717I) mutations. Founder animals (line J1.96) carry a single copy of the transgene. Hemizygous animals are viable and fertile and express mutant human APP mRNA at levels comp
RESEARCH MODELS Summary These transgenic mice express a chimeric mouse/human APP carrying the Swedish mutation under the control of the mouse prion protein promoter. This line, E1-2, was generated in parallel with line C3-3 which also expresses APP with the Swedish mutat
RESEARCH MODELS Modification Details Construct encodes a fusion protein of the BRI protein and Aβ40 driven by the mouse prion promoter; Aβ40 is secreted through proteolytic cleavage of the protein at a furin cleavage site immediately preceding Aβ40. Summary These transge
RESEARCH MODELS Summary These transgenic mice overexpress Aβ42 without overexpressing APP. They contain a fusion construct of the BRI protein, which is involved in amyloid deposition in Familial British Dementia (FBD) and Familial Danish Dementia (FDD), and Aβ42. Twenty-
RESEARCH MODELS These mice express human APP driven by the mouse prion protein promoter. Hemizygous mice are viable and fertile, but phenotypic information is not available. Mouse Alzheimer's Disease Unknown. Jackson Labs: Stock# 006006; Cryopreserved Unknown. Trans
RESEARCH MODELS Summary These knock-in mice, commonly called ADF, carry an insertion incorporating parts of exon 16 and exon 17 of APP. Homozygotes are viable and fertile. No overt phenotype has been observed. Modification Details The targeting vector incorporates a wild
RESEARCH MODELS Summary The endogenous APP gene was disrupted in these animals by homologous recombination. At birth, mice homozygous for the targeted allele are viable and do not display any gross physical or behavioral abnormalities. No APP gene product (mRNA or protei
RESEARCH MODELS Summary These mice have a targeted deletion of the Amyloid β (A4) precursor-like protein 2 (APLP2), a member of the APP gene family with sequence homology to APP. No APLP2 gene product (mRNA or protein) is detected in homozygous null animals. Homozygous n
RESEARCH MODELS Summary These mice have a targeted deletion of part of the mouse β-site APP-cleaving enzyme 2 (BACE2) gene. In contrast to animals with targeted deletion of BACE1, homozygous BACE2 null animals are viable, fertile, normal in size and do not display any gr
RESEARCH MODELS Summary These mice have a targeted deletion in the mouse gene β-site APP cleaving enzyme 1 (BACE1). Homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No BACE1 protein is detected by Wes
RESEARCH MODELS Summary Targeted gene replacement was used to replace the endogenous murine APOE gene with the human APOE2 allele. In humans, the APOE2 allele is associated with decreased risk of Alzheimer's disease and an increased risk for type III hyperlipoprotei
RESEARCH MODELS Modification Details Inactivation of the endogenous mouse APOE by homologous recombination and insertion of a neomycin cassette. Other Phenotypes ApoE is undetectable in the plasma of these homozygous APOE knock-out mice. They are viable and appear health
RESEARCH MODELS These transgenic mice express wild-type human APP under the control of the human PDGF-β promoter. They were generated as control mice for the J20 model. They express human APP in neurons throughout the brain, with maximal levels in the neocortex and hippo
RESEARCH MODELS Summary These mice express human apolipoprotein E4 (APOE4) driven by the human glial fibrillary acidic protein (GFAP) promoter in the absence of endogenous mouse APOE. Human ApoE4 protein is detectable in glia and neuropil in a pattern that is similar to
