Transgenic Amyloid Models

Test putative Alzheimer’s disease therapeutics using in vivo models with amyloid beta plaque deposition and the downstream pathological events

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Home » Neurology Research Models and Services  » Alzheimer’s models and services » Alzheimer’s models – Transgenic Amyloid Models

The histopathological hallmarks of Alzheimer’s disease (AD) are extracellular plaques composed of Amyloid Beta (Aβ) and intracellular inclusions of the protein Tau (neurofibrillary tangles). Cleavage of the amyloid precursor protein (APP) leads to the generation of amyloid beta (Aβ) protein fragments. 

Mouse models of amyloid pathology (over)express the human APP with familial AD-related mutations. These mouse models recapitulate the Aβ aggregation cascade by expressing higher levels of the toxic Aβ1-40 and Aβ1-42 peptides. The biological and associated behavioural deficits observed in amyloid models make them a valuable model of AD, suitable for drug-screening studies.

InnoSer offers unique contract research services using several in vivo AD models, including a range of transgenic Aβ models. Transgenic Aβ models faithfully recapitulate AD’s Aβ plaque pathology. Transgenic Aβ models can be used to study downstream pathological events such as neuroinflammation. As all transgenic models present with amyloid plaques, inflammation and cognitive deficits in different timeframes; the choice of the model depends on experimental compound’s mechanism of action and your research goals.  

Take advantage of InnoSer’s expertise, flexibility and collaborative approach for your research. Our in-house neurology experts have a long-standing experience with modelling AD in vivo and are happy to help guide your decision on choosing the best model fit for your current research goals. 

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Transgenic amyloid models that InnoSer offers:

  • APP/PS1 (ARTE10)
  • APPSWE (Tg2576)
  • APPSWE-Tau
  • Humanized APP (APP-SAA Targeted Replacement)

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Compare our model capabilities and discover which of our neurology platforms suits your research needs

Neurology platform overview
Belgian based preclinical neurology CRO mouse models

Key readouts

Test the efficacy of your treatments in the following battery of cognitive behavioural tests:

  • CognitionWall Discrimination learning
  • Morris water maze
  • 8-arm radial maze test
  • Fear conditioning
  • Nesting test
  • T maze spontaneous alteration.
Behavioural tests catalogue
Test the efficacy of your treatments with the following biological readouts: 

  •  MSD: Plasma, CSF, and brain (e.g., Aβ, cytokines, NfL). 
  • (Digital) histopathology 
  • Immunohistochemistry (e.g., Aβ plaques, phosphorylated Tau, microglia & astrocyte activation)
  • Immunofluorescence and FISH 

Amyloid mouse models show an impaired cognitive performance during the CognitionWall™ Discrimination learning

This deficit is already apparent at 12 weeks of age, before the appearance of plaques (~26 weeks). At 16 weeks, this deficit in discrimination learning can be rescued by an acute dose of the BACE1 inhibitor LY2886721. Using the CognitionWall™, we developed a one-night automated test to efficiently identify discrimination learning impairments in mice, without time-consuming handling of mice. The CognitionWall™ is a wall with three entrances in front of a food dispenser. Mice are rewarded with a food reward when they choose to pass through one of the three entrances. The rate at which a mouse gains a relative preference for the rewarded entrance is used as a measure of discrimination learning. 

BACE1 inhibitors lower Aβ levels in plasma and brain

The number and size of amyloid plaques and associated neuroinflammation can be quantified after immunohistochemical (IHC) staining of brain slices. Aβ levels can be quantified in the brain, cerebrospinal fluid, and blood using ultra-sensitive immunoassays.

ARTE10 mice show progressive Aβ plaques (X04) and astrogliosis

In ARTE10 mice, methoxy-X04-positive amyloid plaque deposition is detected at 6 months (6M) of age, which becomes more pronounced at 10 months of age (10M). This is associated with reactive astrocytes (GFAP) around the plaques.

Reactive microglia around plaques in ARTE10 mice

Iba1 (general microglia marker), shows clusters of microglia in ARTE10 mice. CD11B (neuroinflammation-related microglia marker) shows increases signal around plaques. MHC-II (neuroinflammation-related microglia marker) shows increased signal around the plaques. 

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InnoSer has earned the AAALAC accreditation, demonstrating our commitment to responsible animal care and use. AAALAC International is a nonprofit organization that promotes the humane treatment of animals in science through voluntary accreditation and assessment programs. Our accreditation is valid for three years, incl. 2023. Read more about the AAALAC accreditation programme here.

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