CX3CR1 and Cognitive impairment: In hAPP mice models, CX3CR1 knockout promoted Tau pathology (hyperphosphorylation) and cognitive deficits with no significant changes in APP processing and levels of Aβ [97], whereas Lee et al., demonstrated that CX3CR1 deficiency regulates Aβ deposition, promotes microglial phagocytosis and Aβ clearance in APPPS-1 and R1.40 mice models [98].