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

Jens Pahnke on Studies Suggest Mitochondria Changes Precede Aging, Alzheimer’s

COMMENT Small changes in the mitochondrial DNA (mtDNA) can lead to severe effects over time. Recently, we have shown that minor base changes in the mtDNA of conplastic mouse strains in the C57Bl/6 genomic background may affect hallmarks of AD (Scheffler et al., 2

Tales of Traveling Tau: Is Transfer Between Neurons Normal?

CONFERENCE COVERAGE 2013-08-27 Conference Coverage A creepy idea is taking hold in Alzheimer’s research. Like a computer worm that travels through networks corrupting perfectly good files, toxic forms of tau bore from neuron to neuron turning good protein into bad along the way. Scient

Jack Muses

United States

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

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

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

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-

BRI-Aβ40 (BRI2-Aβ40)

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