Fig. 3: AdipoRon rescues mitochondrial deficits caused by tauopathy.
From: Reversal of neuronal tau pathology via adiponectin receptor activation
A mRNA abundance of Ppargc-1a isoforms was determined by RT-qPCR (n = 6–8 mice per treatment per genotype). B Representative images of mitochondria detected with TOMM20 antibody. C Quantification of mitochondrial size, (D) Integrated density, and (E) circularity (n = 6 mice per genotype, n = 23–59 cells neurons per treatment per genotype. F Mitochondrial membrane potential (JC-1) 2 h after 10 µM AR treatment (n = 5–6 mice per genotype; n = 30–43 observations per genotype per treatment). G Relative ATP concentrations after 12 h of AdipoRon treatment (n = 8–12 mice per genotype, n = 26–41 observations per treatment per genotype). H Heatmap of log2FC of fatty acid metabolism GSEA pathway genes in AR-treated WT and Tau neurons with Tau compared to WT included for reference. I Representative images of LipidTox dye (scale bar 15 µM). J, K Quantification of lipid droplet size and total area (n = 5 mice per genotype, n = 30–55 neurons per treatment per genotype). Significance determined by multiple Student’s t-test or two-way ANOVA with Tukey’s multiple comparisons test. Data shown as mean ± SEM *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
