Figure 5.
Fibrin(ogen) deposition is decreased in AD mice treated with FXII-ASO. Brain sections from WT and AD mice treated with CTL-ASO or FXII-ASO were stained with an antibody against fibrin(ogen) (A-D), blood vessels were visualized by lectin staining (E-H), and the images were merged (I-L). CTL-ASO–treated AD mice showed significantly more fibrin(ogen) staining (C) than CTL-ASO–treated WT mice (A). In FXII-ASO–treated AD mice, fibrin(ogen) deposition was significantly reduced (D,L,M) compared with CTL-ASO–treated AD mice (C,K,M). Fibrin(ogen) deposits were minimal in WT mice and were similar between CTL-ASO (A,I,M) and FXII-ASO treatments (B,J,M) (one-way ANOVA; n = 9-14 mice per group). All values presented as mean ± SEM. Results are from 3 independent experiments. Scale bar for panels A-L, 100 μm.

Fibrin(ogen) deposition is decreased in AD mice treated with FXII-ASO. Brain sections from WT and AD mice treated with CTL-ASO or FXII-ASO were stained with an antibody against fibrin(ogen) (A-D), blood vessels were visualized by lectin staining (E-H), and the images were merged (I-L). CTL-ASO–treated AD mice showed significantly more fibrin(ogen) staining (C) than CTL-ASO–treated WT mice (A). In FXII-ASO–treated AD mice, fibrin(ogen) deposition was significantly reduced (D,L,M) compared with CTL-ASO–treated AD mice (C,K,M). Fibrin(ogen) deposits were minimal in WT mice and were similar between CTL-ASO (A,I,M) and FXII-ASO treatments (B,J,M) (one-way ANOVA; n = 9-14 mice per group). All values presented as mean ± SEM. Results are from 3 independent experiments. Scale bar for panels A-L, 100 μm.

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