Species: Mouse
Genes: APP
Mutations: APP K670_M671delinsNL (Swedish)
Modification: APP: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: B6.D2-Tg(Thy1-APPSwe)71Blt; B6.D2-Tg(Thy1-APPSwe)72Blt
Genetic Background: C57BL/6, DBA/2, crossed to C57BL/6
Availability: Available through Laurence Ozmen

Neuropathology

Amyloid plaques by 17-18 months in the neocortex and hippocampus with detection of five to ten-fold more Aβ40 than Aβ42. Plaque burden significantly lower than in the double transgenic PS2APP. Lower levels of insoluble Aβ40 and Aβ42 than the PS2APP mouse at 16-18 months (Richards et al., 2003).

Cognition/Behavior

Unknown.

Modification Details

Transgene with human APP (isoform 751) with the Swedish mutation driven by the Thy1.2 promoter.

The parental origin of the transgenes was shown to influence AD-related pathology in another model, 5xFAD (C57BL6), in which the Thy1 promoter drives transgene expression, possibly due to genomic imprinting of the promoter (Sasmita et al.,  2025). While this phenomenon has not yet been demonstrated in APPSwe mice, users of this model should be aware of the findings in 5xFAD mice when designing and documenting breeding strategies.

Note

This line of mutant APP mice was used to generate a double transgenic animal, PS2APP, by breeding to PS2(N141I) mice (Richards et al., 2003). The construct used to generate these mice was also co-injected with the construct expressing PSEN2(N141I) into C57Bl/6 zygotes to generate another double transgenic line, 152H, which is also known as PS2APP (Ozmen et al., 2009).

Availability

Contact Laurence Ozmen.

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References

Research Models Citations

1. PS2APP (PS2(N141I) x APPswe)
2. 5xFAD (C57BL6)
3. PS2(N141I)
4. PS2APP

Paper Citations

1. Richards JG, Higgins GA, Ouagazzal AM, Ozmen L, Kew JN, Bohrmann B, Malherbe P, Brockhaus M, Loetscher H, Czech C, Huber G, Bluethmann H, Jacobsen H, Kemp JA. PS2APP transgenic mice, coexpressing hPS2mut and hAPPswe, show age-related cognitive deficits associated with discrete brain amyloid deposition and inflammation. J Neurosci. 2003 Oct 1;23(26):8989-9003. PubMed.
2. Sasmita AO, Ong EC, Nazarenko T, Mao S, Komarek L, Thalmann M, Hantakova V, Spieth L, Berghoff SA, Barr HJ, Hingerl M, Börensen F, Hirrlinger J, Simons M, Stevens B, Depp C, Nave KA. Parental origin of transgene modulates amyloid-β plaque burden in the 5xFAD mouse model of Alzheimer's disease. Neuron. 2025 Jan 20; Epub 2025 Jan 20 PubMed.
3. Ozmen L, Albientz A, Czech C, Jacobsen H. Expression of transgenic APP mRNA is the key determinant for beta-amyloid deposition in PS2APP transgenic mice. Neurodegener Dis. 2009;6(1-2):29-36. PubMed.

Other Citations

1. Laurence Ozmen

Further Reading