Figure 6.
Depletion of plasma FXII reduces inflammation-associated neuronal damage in AD mouse brains. Brain sections from CTL-ASO- or FXII-ASO–treated WT and AD mice were stained with antibodies against CD11b (A,D,G,J) and Tuj1 (B,E,H,K), and the images were merged (C,F,I,L). In CTL-ASO–treated AD mice, the staining for Tuj1 was weaker in areas where CD11b staining was robust (G,H,I), indicating microglia/macrophage-associated neuronal damage. This microglia/macrophage-associated neuronal damage was significantly reduced in FXII-ASO–treated AD mice (J-M) compared with CTL-ASO–treated AD mice (G,H,I,M) There were no detectable microglia/macrophage-associated changes in Tuj1 staining in either CTL-ASO- or FXII-ASO–treated WT mice (A-F). Student t test, n = 10/group. All values presented as mean ± SEM. Results are from 3 independent experiments. Scale bar for panels A-L, 100 μm.

Depletion of plasma FXII reduces inflammation-associated neuronal damage in AD mouse brains. Brain sections from CTL-ASO- or FXII-ASO–treated WT and AD mice were stained with antibodies against CD11b (A,D,G,J) and Tuj1 (B,E,H,K), and the images were merged (C,F,I,L). In CTL-ASO–treated AD mice, the staining for Tuj1 was weaker in areas where CD11b staining was robust (G,H,I), indicating microglia/macrophage-associated neuronal damage. This microglia/macrophage-associated neuronal damage was significantly reduced in FXII-ASO–treated AD mice (J-M) compared with CTL-ASO–treated AD mice (G,H,I,M) There were no detectable microglia/macrophage-associated changes in Tuj1 staining in either CTL-ASO- or FXII-ASO–treated WT mice (A-F). Student t test, n = 10/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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