Depletion of plasma FXII reduces astrocyte activation in the AD mouse brain. (A-E) Brain sections from WT and AD mice treated with CTL-ASO or FXII-ASO were stained with an antibody against GFAP (A-D), and the cerebral cortex was analyzed (E). CTL-ASO–treated AD mice showed significantly higher expression of GFAP (C,E) than CTL-ASO–treated WT mice (A,E). In FXII-ASO–treated AD mice, GFAP (D) was significantly reduced compared with CTL-ASO–treated AD mice (C,E). GFAP expression was similar between CTL-ASO–treated (A,E) and FXII-ASO–treated (B,E) WT mice (one-way ANOVA; n = 9-14 mice per group). Scale bar for panels A-D, 100 μm. (F-G) Western blot analyses of hippocampal extracts from WT and AD mice treated with CTL-ASO or FXII-ASO revealed that the expression level of GFAP was significantly higher in CTL-ASO–treated AD mice than in CTL-ASO–treated WT mice. FXII-ASO treatment significantly reduced GFAP expression in AD mice when compared with CTL-ASO treatment. The expression level of GFAP was similar between WT mice treated with FXII-ASO or CTL-ASO (one-way ANOVA; n = 9-14 mice per group; shown here are representative western blots). All values presented as mean ± SEM. Results are from 3 independent experiments.