While our previous studies have shown that a deletion of Cx3cr1 in B6 mice augments microglial uptake of exogenously injected Aβ42 [25], the role of CX3CR1 in microglial phagocytosis of endogenously produced, extracellular fAβ plaques in the context of accumulating AD pathology is largely unclear. This evidence concerns the gene CX3CR1 and Alzheimer disease.