Fig 1: Effect of UA on mitochondrial dysfunction, neuroinflammation, and DNA damage. (A) Representative western blots showing PINK1, Parkin, STAT3, p‐STAT3, NLRP3, AIM2, and Bax in the hippocampus of WT, AD, and ADP mice with/without UA; n = 3 mice per group (1 F and 2 M). (B–G) Quantitation of protein levels for indicated proteins in Figure 6A. (H–I) Representative western blots showing PAR, p‐Parkin, and γH2AX expression in the hippocampus and γH2AX quantification; n = 5 mice per group. (J–L) Representative western blots showing Ctsw and Ctsd and the quantitation of these protein levels in the hippocampus of WT, AD, and ADP mice with/without UA; n = 3 mice per group (1 F and 2 M). (M, N) Ctsz and Ctsw levels by ELISA assay. (O, P) Representative western blots showing Ctsz and the quantitation of the protein levels in the hippocampus of WT, AD, and ADP mice with/without UA, n = 5 mice per group. For H and O, WT (2 M & 3 F), AD (3 M & 2 F), AD+UA (3 M & 2 F), ADP (3 M & 2 F), and ADP+UA (2 M & 3 F). F, female, M, male. All bands were normalized to their respective loading controls β‐actin. Error bars represent the mean ± SEM. Data were analyzed by one‐way ANOVA analysis of variance with Tukey's multiple comparisons test (B–G, I, K–N, P).