For instance, neutralizing antibodies against (brain) CX3CR1 ameliorated exogenous CX3CL1-induced PD-like behaviors in an adult rat model [250], while another study in a mouse model of PD revealed the neuroprotective capacity of CX3CL1 that resides solely upon the soluble form but not the membrane-located form of CX3CL1 [251]. This evidence concerns the gene CX3CR1 and Parkinson disease.