Overall, the interactions proposed in the mechanistic hypothesis in Fig. 6 could explain the key role of microglial NLRP3 inflammasome activation in PD-related α-syn pathology, neuroinflammation, and dopaminergic neurodegeneration described by others [12, 69], and offer a potential mechanistic basis for the particular vulnerability of SN dopaminergic neurons in PD. This evidence concerns the gene NLRP3 and Parkinson disease.