This study was conceived based on previous data showing increased microglia activation in mice lacking CX3CR1 and in which a predominance of proinflammatory mediators correlated with neurotoxicity in the brain in models of low-level endotoxemia, Parkinson’s disease, and Amyotrophic lateral sclerosis (Cardona et al., 2006b). This evidence concerns the gene CX3CR1 and Parkinson disease.