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). Here, CX3CL1 is linked to Parkinson disease.