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. Author manuscript; available in PMC: 2016 Feb 4.
Published in final edited form as: Neuron. 2015 Jan 22;85(3):534–548. doi: 10.1016/j.neuron.2014.12.068

Figure 1. Il10 deficiency reduces cerebral amyloidosis in APP/PS1 mice.

Figure 1

(A) Representative micrographs of amyloid plaques labeled with thioflavinS from the cingulate cortex (CC), entorhinal cortex (EC) and hippocampus (HC) of APP/PS1 mice homozygous, heterozygous or completely deficient for Il10. Scale bar denotes 100 µm. (B, C) Quantitation of thioflavinS (B) and 4G8 (C) labeling.

(D) Semi-quantitative analysis of cerebral amyloid angiopathy severity (CAA score) from thioflavinS-labeled brain sections.

(E–H) ELISA analysis of frontal cortex detergent-soluble (E, F) or guanidine-HCl-extracted (G, H) Aβ1–40 and Aβ1–42 species from mice with the indicated genotypes. For (B–H), data are presented as mean ± SEM for APP/PS1+Il10+/+ (n=10–18), APP/PS1+Il10+/− (n=9–24), and APP/PS1+Il10−/− mice (n=3–10); * p<0.05, ** p<0.01, *** p<0.001.

(I) Western blots of human (h) APP or hPS1 levels in frontal cortex homogenates of APP/PS1 mice with the indicated genotypes. Beta-actin is shown as a loading control.

(J) Quantitation of hAPP or hPS1 protein levels in frontal cortex homogenates from APP/PS1 mice of the indicated genotypes. Expression levels are normalized to β-actin. Data are represented as mean ± SEM for n=6 samples for each group, with APP/PS1+Il10+/+ signal normalized to 100%; non-significant.

(K) Q-PCR analysis of APP and PS1 mRNA levels in frontal cortex from mice with the indicated genotypes. The mRNA levels are normalized to HPRT, and n=6 per group; non-significant. See also Figure S1.