Knockout of Cx3cr1 in a toxin-induced model of Parkinson’s disease (PD) and a genetic model of Amyotrophic Lateral Sclerosis (ALS) (Tg SOD1G93A) worsened the phenotype, in both cases producing more neuronal loss and, for the ALS model, accelerated deterioration of hind limb grip function and reduced survival were also seen [9]. Here, CX3CR1 is linked to amyotrophic lateral sclerosis.