Research Models

tg-APPSwe

Synonyms: Tg-Swe

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Species: Mouse
Genes: APP
Mutations: APP K670_M671delinsNL (Swedish)
Modification: APP: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
Genetic Background: C57BL/6J
Availability: Available through Lars Nilsson

Neuropathology

Extracellular amyloid deposition begins at approximately 12 months of age (Philipsson et al., 2009) whereas intraneuronal Aβ aggregates occur at approximately six months (Lord et al., 2006). Extracellular pathology, both cerebrovascular amyloid angiopathy (CAA) and congophilic parenchymal plaques, are mainly found in the cerebral cortex, hippocampus and thalamus. Aβ-burden in cerebral cortex is approximately one percent at 12 months and 2.8 percent at 18 months (Lord et al.,  2011).

Cognition/Behavior

Unknown.

Modification Details

Transgene with human APP (isoform 695) bearing the Swedish mutation under the murine Thy1 promoter.

Related Model

This model was originally described in conjunction with a model expressing APP bearing both the Swedish and Arctic mutations (Tg-ArcSwe), which has a more severe phenotype (Lord et al., 2006).

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

  • Tangles
  • Neuronal Loss

No Data

  • Synaptic Loss
  • Changes in LTP/LTD
  • Cognitive Impairment

Plaques

Plaques are detectable at approximately 12 months and are heterogeneous in morphological structure and size, as well as in terms of fluorescence emitted when stained with luminescent polymers (conformational amyloid ligands)(Philipsson et al., 2009).

Tangles

Absent.

Neuronal Loss

Absent.

Gliosis

Microgliosis and astrogliosis are most prominent in the hippocampus, but also found locally around deposits in the cerebral cortex and in thalamus at approximately 12 months (Philipsson et al., 2009).

Synaptic Loss

Unknown.

Changes in LTP/LTD

Unknown.

Cognitive Impairment

Unknown.

Last Updated: 16 Jul 2018

COMMENTS / QUESTIONS

  1. Further evidence for the heterogeneity of protein aggregates, and a reminder that each transgenic model may have specific pathologic characteristics that should be considered when selecting a model for experimental purposes.

    View all comments by Lary Walker

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References

Research Models Citations

  1. Tg-ArcSwe

Paper Citations

  1. Philipson O, Hammarström P, Nilsson KP, Portelius E, Olofsson T, Ingelsson M, Hyman BT, Blennow K, Lannfelt L, Kalimo H, Nilsson LN. A highly insoluble state of Abeta similar to that of Alzheimer's disease brain is found in Arctic APP transgenic mice. Neurobiol Aging. 2009 Sep;30(9):1393-405. PubMed.
  2. Lord A, Kalimo H, Eckman C, Zhang XQ, Lannfelt L, Nilsson LN. The Arctic Alzheimer mutation facilitates early intraneuronal Abeta aggregation and senile plaque formation in transgenic mice. Neurobiol Aging. 2006 Jan;27(1):67-77. PubMed.
  3. Lord A, Philipson O, Klingstedt T, Westermark G, Hammarström P, Nilsson KP, Nilsson LN. Observations in APP bitransgenic mice suggest that diffuse and compact plaques form via independent processes in Alzheimer's disease. Am J Pathol. 2011 May;178(5):2286-98. PubMed.

Other Citations

  1. Lars Nilsson

Further Reading

No Available Further Reading