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BRI-Aβ42 (BRI2-Aβ42)

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-

Prnp-APP

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

APP Knock-in

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

APP Knock-out

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

APLP2 Knock-out

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

BACE2 Knock-out

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

BACE1 Knock-out

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

APOE2 Targeted Replacement

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

APOE Knock-out

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

PDGF-APP(WT) (line I5)

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

GFAP-APOE4/APOE Knock-out

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

TetO-APPSweInd (line 885)

RESEARCH MODELS Summary This model enables regulated expression of mutant APP using a tet-off system. The APP transgene bears both the Swedish and Indiana mutations under the control of a tetracycline-responsive promoter. When bred to transgenic mice expressing reverse t

TetO-APPSweInd (line 102)

RESEARCH MODELS Summary These mice enable regulated expression of mutant APP using a tet-off system. A tetracycline-responsive promoter drives expression of the APP transgene which carries the Swedish and Indiana mutations. When bred to transgenic mice expressing reverse

Ts65Dn

RESEARCH MODELS Summary This well-characterized model of Down's syndrome develops elevated APP but lacks appreciable β-amyloid pathology. The mice are aneuploid and carry the translocation chromosome, Mmu17 16 (17 16), as a freely segregating, supernumerary chromoso

PSEN1 Knock-out

RESEARCH MODELS Summary These mice are deficient in PSEN1. This model is perinatal lethal in homozygouse animals which die shortly after birth, presumably from breathing difficulties due to ribcage deformity (Shen et al., 1997). Gross skeletal malformations and central n

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