Amyloid and Tau mouse models recapitulate pathological processes found in patients with Alzheimer’s Disease (AD), including protein aggregation, neuroinflammation, neurodegeneration, and cognitive impairments.
The key to understanding a therapeutic compound’s effect on amyloid-beta (Aβ) pathology-induced neuroinflammation, is to use robust and reliable models that consistently show progressive plaque pathology. The APP/PS-1 (ARTE10) proves to be such a model, allowing a reliable semi-quantification of the spatial distribution and density of Aβ plaques, as well as different neuroinflammation markers. In turn, this enables the testing of novel therapies (for e.g., amyloid-lowering compounds).
As seen in the immunofluorescent image above, we detect clear and progressive (6 vs 10 months, ****P<0.0001) pathologic Aβ plaque deposition (Methoxy-X04+) accompanied by clusters of reactive astrocytes (GFAP+) in the cortex of the ARTE10 mouse model.
In line, we observe that the Aβ-directed monoclonal antibody Aducanumab stimulates microglial phagocytosis (HMC3 cell line) following incubation with pHRODO-labelled Aβ fibrils (*P<0.05; ***P<0.001; ****P<0.0001).
To help you fine-tune your lead compound’s bioavailability, InnoSer has ample experience in carrying out PK/PD studies and analyses. To ensure your compound’s safety, InnoSer can additionally perform safety pharmacology analyses.
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