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). This evidence concerns the gene CX3CL1 and amyotrophic lateral sclerosis.