Further supporting a potential role for CX3CR1 signaling in AD pathogenesis, Lee et al. (2010) reported that in two different mouse models of AD (APPS1 and R1.40), characterized by different velocity of β-amyloid deposition, crossing with cx3cr1-/- mice reduced the extent of amyloid deposition, the number of dystrophic neurons and of plaque-associated microglia cells. Here, CX3CR1 is linked to Alzheimer disease.