Research Models

APPSwe (line C3-3)

Synonyms: APP(695)Swe

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Species: Mouse
Genes: APP
Mutations: APP K670_M671delinsNL (Swedish)
Modification: APP: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: C3B6-Tg(APP695)3Dbo/Mmjax
Genetic Background: C3H/HeJ x C57BL/6J; backcrossed to C57BL/6J
Availability: The Jackson Lab; available through the JAX MMRRC Stock# 034828; Cryopreserved

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, C3-3, was generated in parallel with line E1-2, which also expresses APP carrying the Swedish mutation. Mice that are hemizygous for the transgene are viable and fertile and express mutant human APP at levels about 3-fold higher than endogenous mouse APP. These mice do not exhibit amyloid plaque deposition until approximately 18 to 20 months of age (Borchelt et al., 1997; Janokowsky et al., 2004). They do not show impairments in standard working and reference memory tasks (Savonenko et al., 2003).

This model was previously available through The Jackson Lab as Stock# 003375.

Modification Details

The transgene is a chimeric mouse/human APP (isoform 695) with a "humanized" Aβ domain and the Swedish mutation under the control of the mouse prion protein promoter.

Related Strains

B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax (see APPSwe/PSEN1dE9)
The Jackson Lab: the JAX MMRRC Stock# 034833 (formerly The Jackson Lab Stock# 005866)

B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J (see APPSwe/PSEN1(A246E)
The Jackson Lab: Stock# 003378

Phenotype Characterization

When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.

Absent

  • Cognitive Impairment

No Data

  • Tangles
  • Neuronal Loss
  • Gliosis
  • Synaptic Loss
  • Changes in LTP/LTD

Plaques

Some plaque formation at advanced age (24-26 months) (Savonenko et al., 2003).

Tangles

No data.

Neuronal Loss

No data.

Gliosis

No data.

Synaptic Loss

No data.

Changes in LTP/LTD

No data.

Cognitive Impairment

Normal reference and working memory up to 12-14 months on congenic background (Savonenko et al., 2003).

Last Updated: 06 Apr 2022

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References

Research Models Citations

  1. APPSwe (line E1-2)
  2. APPSwe/PSEN1(A246E)

Paper Citations

  1. Borchelt DR, Ratovitski T, van Lare J, Lee MK, Gonzales V, Jenkins NA, Copeland NG, Price DL, Sisodia SS. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins. Neuron. 1997 Oct;19(4):939-45. PubMed.
  2. Jankowsky JL, Fadale DJ, Anderson J, Xu GM, Gonzales V, Jenkins NA, Copeland NG, Lee MK, Younkin LH, Wagner SL, Younkin SG, Borchelt DR. Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. Hum Mol Genet. 2004 Jan 15;13(2):159-70. Epub 2003 Nov 25 PubMed.
  3. Savonenko AV, Xu GM, Price DL, Borchelt DR, Markowska AL. Normal cognitive behavior in two distinct congenic lines of transgenic mice hyperexpressing mutant APP SWE. Neurobiol Dis. 2003 Apr;12(3):194-211. PubMed.

Other Citations

  1. line E1-2,

External Citations

  1. The Jackson Lab: the JAX MMRRC Stock# 034833
  2. The Jackson Lab: Stock# 003378
  3. JAX MMRRC Stock# 034828

Further Reading