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Model Overview

β-amyloid pathology is a hallmark of Alzheimer's disease. While multiple transgenic models of β-amyloid pathology exist, they each have their respective strengths and weaknesses.

At Biospective, we have validated the ARTE10 (APP/PS1) transgenic mouse model. Significant advantages of this model include:

  • β-amyloid plaque formation beginning around 3 months-of-age, with a time-dependent increase in burden and extent
  • Fibrillar extracellular and intracellular pathology
  • Parenchymal and vascular β-amyloid pathology
  • Robust astrogliosis and microgliosis
  • Brain and spinal cord pathology

The model time course is predictable and the measures are highly reproducible.

These mice are readily available at Biospective at ages appropriate for preclinical therapeutic studies.

Model Generation

ARTE10 [C57BL/6NTac.CBA-Tg(Thy1-PSEN1*M146V,-APP*Swe)10Arte] homozygous mice are generated on a C57BL/6NTac background. ARTE10 is a transgenic line with two co-integrated constructs: Thy-1 promoter specific expression the transgene coding for the 695-amino acid isoform that harbors the Swedish mutation of human Alzheimer β-amyloid (Aβ) precursor protein (APPsw), as well as human Presenilin 1 carrying the M146V mutation (PS1M146V). The model expresses high concentrations of human Aβ protein, and develops human Alzheimer's disease-like amyloid pathology due to genetic mutations within the human APP and PSEN1 genes. The model has been used for non-invasive imaging of β-amyloid plaques using Amyloid PET imaging tracers.

Our Validated Measures

Multiplex immunofluorescence staining (β-amyloid, Iba-1, GFAP) from a 9 month-old APP/PS1 mouse.

Time-dependent β-amyloid plaque formation in the frontal cortex.

Learn more about our characterization of this model and our validated measures.

Discover more of our Alzheimer's Models


At what age are β-amyloid plaques initially seen?

β-amyloid plaques are initially found in the frontal cortex at ~3 month-of-age.

What type of neuroinflammation is seen in the β-amyloid transgenic model?

We observe a very interesting spatiotemporal pattern of microgliosis (including activated microglia) and astrogliosis in this model. We have performed a detailed analysis, which can be found in our Presentation - β-amyloid & the inflammatory microenvironment in an APP/PS1 mouse model of Alzheimer's disease.

Is cerebral amyloid angiopathy (CAA) seen in the β-amyloid transgenic model?

We see extensive β-amyloid vascular pathology in this model. Amyloid staining can readily be observed in the leptomeningeal and deeper parenchymal blood vessels.

What promoter is used for transgene expression in the β-amyloid transgenic model?

The mutant human APP and PSEN1 transgenes are expressed under control of the Thy-1 promoter.

What areas of the brain show β-amyloid plaques in the β-amyloid transgenic mouse model?

Plaques are initially found in the frontal cortex and subiculum. As the mice age, there is a well-defined spatiotemporal pattern of β-amyloid pathology with extensive plaque burden in many brain regions, including the hippocampus and thalamus. We have performed a thorough characterization of this model from 3 to 15 months-of-age.

More Information

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