Fibrillar Aβ causes profound microglial metabolic perturbations in a novel APP knock-in mouse model.

Altogether, our in-depth analysis of the App knock-in mouse model confirms emergence of disease-relevant biology and progressive accumulation of pathological hallmarks of AD. Our data lends further support to the notion that phagocytic microglia undergo profound cellular alterations, including lysosomal dysfunction, lipid dyshomeostasis, and other metabolic changes. Since this new mouse model can be used to investigate multiple relevant aspects of AD biology, we have made it broadly available to the scientific community.