Fig. 2
From: Terminal complement pathway activation drives synaptic loss in Alzheimer’s disease models
Complement activation products in wildtype and AppNL−G−F mouse synaptoneurosomes (SN). a C1q levels were significantly increased in AppNL−G−F synaptoneurosomes (SN) at 6, 9 and 12 months (m) compared to age-matched wildtype (WT) (n = 5–8). SN C1q levels were significantly increased between 6 to 9 months, and 9 to 12 months in WT and between 9 to 12 months in AppNL−G−F SN. One-way ANOVA with Tukey’s post-hoc test was used to test significance of differences between age groups of each genotype (dashed horizontal lines). Two-way ANOVA with Bonferroni post-hoc test was used to compare between genotypes at each age solid horizontal lines. b Representative western blot confirming increased C1q levels in TBH and SN in AppNL−G−F compared to WT mice. Alpha-tubulin was used as loading control and C1q-deficient TBH and SN were included as controls. c TCC levels were significantly increased in AppNL−G−F SN at 6, 9 and 12 months compared to WT (n = 5–8). TCC levels in SN remained stable with increased age in WT mice but were significantly increased at 9 and 12 months compared with 3 months in AppNL−G−F. One-way ANOVA with Tukey’s post-hoc test was used to test for differences between age groups of each genotype (dashed horizontal lines). Two-way ANOVA with Bonferroni post-hoc test was used to compare between genotypes at each age (solid horizontal lines). Error bars correspond to SEM. **P < 0.01, ***P < 0.001, ****P < 0.0001