Fig. 7
From: Neuronal transcriptome, tau and synapse loss in Alzheimer’s knock-in mice require prion protein
PrPC mediates the localization of C1q to PSD-95 puncta without altering C1q levels. A Anti-C1q immunoblot image of cortical brain lysates from 20-month-old WT, Prnp−/−, DKI and DKI; Prnp−/− mice. A cropped region of the blot with migration of appropriate Mol Wt markers is shown at left. B Quantification of C1q protein levels from densitometric analysis of immunoblots as in A. DKI animals exhibit significantly increased C1q expression compared to WT. The C1q level in DKI; Prnp−/− mice does not differ from DKI group values. Data are graphed as mean ± SEM, analyzed by ordinary one-way ANOVA with Dunnett’s multiple comparisons test, P > .05, **P < .01, n = 10 for WT, n = 10 for Prnp−/−, n = 10 for DKI, and n = 9 for DKI; Prnp−/−. C Representative images of PSD-95 (green) and C1q (red) immunoreactivity in sections of CA1 hippocampus of 10-month-old old WT, Prnp−/−, DKI and DKI; Prnp−/− mice. Scale bar = 1.25 μm. D Quantification of the fraction of PSD-95 immunoreactivity overlapping C1q demonstrates a significant increase in the marking of synapses by C1q in DKI animals compared to WT and WT prnp−/− mice that are significantly decreased by Prnp gene knockout. Data are graphed as mean ± SEM, analyzed by ordinary one-way ANOVA with Tukey’s multiple comparisons test, *P < 0.05, ***P < 0.001, ****P < 0.0001, n = 8 for WT, n = 10 for Prnp−/−, n = 12 for DKI, and n = 12 for DKI; Prnp−/−. E Representative images of PrPC (green) and C1q (red) immunoreactivity in CA1 of 10-month-old WT and DKI mice. Scale bar = 5 μm. F Quantification of the fraction of PrPC immunoreactivity overlapping C1q demonstrates a significant increase in the colocalization of PrPC and C1q in DKI samples compared to WT brain. Data are graphed as mean ± SEM, analyzed by unpaired t test, **P < 0.01, n = 19 for WT, n = 20 for DKI