Transgenic Amyloid Models
Test putative Alzheimer’s disease therapeutics using in vivo models with amyloid beta plaque deposition and the downstream pathological events
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.
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.
Transgenic amyloid models that InnoSer offers:
- APP/PS1 (ARTE10)
- APPSWE (Tg2576)
- Humanized APP (APP-SAA Targeted Replacement)
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Test the efficacy of your treatments in the following battery of cognitive behavioural tests:
- 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.
Related Alzheimer’s disease model options
Neurology Platform Overview
Transgenic Tau Models
Tau Seeding Model
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