CX3CL1 and Alzheimer disease: Loss of this dampening down of microglial activation via the CX3CL1/CX3CR1 interaction may account for the increase in neurotoxicity in mouse models of both Alzheimer disease, Parkinson disease, prion disease, and amyotrophic lateral sclerosis, which lack CX3CR1 (23, 39, 43–45).