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 parallel to this model, we established an in vitro model of Aβ pathology that can be used to study the efficacy of novel compounds in inducing microglial phagocytosis as a putative AD therapy.

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).