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. 2020 Jul 17;17:213. doi: 10.1186/s12974-020-01866-6

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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