Initial work disrupting FKN signaling in animal models (receptor or ligand knockouts) demonstrated increased Parkinson’s disease pathology, tauopathy, and amyotrophic lateral sclerosis (Bhaskar et al. 2010; Cardona et al. 2006), suggesting that dysregulation of microglial activation can result in worsening of disease pathology and neurodegeneration. This evidence concerns the gene CX3CL1 and tauopathy.