Fig. 1

Longitudinal model of mice expressing hyperactive Nlrp3 mutations under the endogenous promotor in DA neurons. a Transgenic mice harboring Cre-driven genetic mutations in Nlrp3, either Nlrp3^A350V, or Nlrp3^L351P, previously associated with the cryopyrin-associated periodic syndromes, were bred with mice harboring IRES-Cre under the control of the Slc6a3 promotor. b Representative genotyping with PCR-based detection of Nlrp3^WT and Nlrp3^mut alleles. Mice double positive for Slc6a3^IRESCre and Nlrp3^mut (Nlrp3^A350V or Nlrp3^L351P) were included in the study as indicated by *, as well as Nlrp3^WT/WT mice as controls. All mice contain one background copy of the Nlrp3^WT gene. c Experimental design of longitudinal study. Histologic sections were analyzed at both 1 month and 18 months of age, and behavior analysis was conducted at the 6, 10, 14, and 18-month time points