huAPP-Aβ Mouse
Product Name
huAPP-Aβ Mouse
Product ID
C002031
Strain Name
C57BL/6JCya-Appem2(hAPP)/Cya
Backgroud
C57BL/6JCya
Status
When using this mouse strain in a publication, please cite “huAPP-Aβ Mouse (Catalog C002031) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
APP
Gene Alias
AAA, AD1, PN2, ABPP, APPI, CVAP, ABETA, PN-II, preA4, CTFgamma, alpha-sAPP
NCBI ID
Chromosome
Chr 21 (Human)
MGI ID
Datasheet
Strain Description
The APP gene encodes the Amyloid Precursor Protein, a type I transmembrane glycoprotein that is ubiquitously expressed but reaches its highest levels in the central nervous system, particularly in the cerebral cortex and hippocampus. Following translation, the APP protein is proteolytically processed via two primary pathways: the non-amyloidogenic pathway, which prevents Aβ formation, and the amyloidogenic pathway, where sequential cleavage by β-secretase (BACE1) and γ-secretase releases amyloid-beta (Aβ) peptides [1]. While its precise physiological role remains an area of active research, APP is known to function in synaptic formation and repair, anterograde neuronal transport, and cell-to-cell adhesion [2]. Pathological mutations or duplications of the APP gene are primary drivers of Alzheimer’s Disease (AD) and Cerebral Amyloid Angiopathy (CAA), characterized by the extracellular accumulation of Aβ plaques and vascular deposits that lead to neurodegeneration and cognitive decline [3].
The huAPP-Aβ mouse is a humanized model constructed via gene editing. The sequences from upstream of exon 16 to downstream of exon 17 of the mouse App were replaced with the sequences from upstream of exon 16 to downstream of exon 17 of the human APP. This model is suitable for studying neurodegenerative diseases such as Alzheimer's disease (AD), as well as for the research, development, and efficacy evaluation of AD therapeutic strategies targeting APP.
Reference
Cole SL, Vassar R. The Alzheimer's disease beta-secretase enzyme, BACE1. Mol Neurodegener. 2007 Nov 15;2:22.
Zheng H, Koo EH. The amyloid precursor protein: beyond amyloid. Mol Neurodegener. 2006 Jul 3;1:5.
Grangeon L, Charbonnier C, Zarea A, Rousseau S, Rovelet-Lecrux A, Bendetowicz D, Lemaitre M, Malrain C, Quillard-Muraine M, Cassinari K, Maltete D, Pariente J, Moreaud O, Magnin E, Cretin B, Mackowiak MA, Sillaire AR, Vercelletto M, Dionet E, Felician O, Rod-Olivieri P, Thomas-Antérion C, Godeneche G, Sauvée M, Cartz-Piver L, Le Ber I, Chauvire V, Jonveaux T, Balageas AC, Laquerriere A, Duyckaerts C, Vital A, de Paula AM, Meyronet D, Guyant-Marechal L, Hannequin D, Tournier-Lasserve E, Campion D; CNR-MAJ collaborators; Nicolas G, Wallon D. Phenotype and imaging features associated with APP duplications. Alzheimers Res Ther. 2023 May 11;15(1):93.
Strain Strategy
The sequences from upstream of exon 16 to downstream of exon 17 of the mouse App were replaced with the sequences from upstream of exon 16 to downstream of exon 17 of the human APP.
Figure 1. Gene editing strategy for huAPP-Aβ mice.
Application Area
Research on Alzheimer's disease (AD);
Research on Cerebral Amyloid Angiopathy (CAA);
Preclinical research such as the development, screening, and efficacy evaluation of APP-targeted therapeutic drugs.
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