CX3CR1 and amyloidosis: Crossing the CX3CR1−/− mice to CRND8 transgenic mice that harbor a gene encoding a mutant human amyloid precursor protein also resulted in reduced Aβ deposits, with the CX3CR1-deficient microglia phagocytosing amyloid plaques and displaying higher proliferation rates in the plaque regions (Liu et al., 2010).