Additional file 7 of Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia

Additional file 7: Supplementary Figure 7. AppSAA knock-in mice have multiple AD pathology-related changes in astrocytes. a Representative images of GFAP and Aβ co-immunolabeling in the CA1 region of the hippocampus (left), and GFAP immunolabeling of entire hemispheres (right) in 18-month-old AppSAA +/+ and AppSAA KI/KI mice. b Representative images of GLT-1 immunolabeling in the CA1 and CA3 subregions of the hippocampus. c Representative images of C3 and GFAP co-immunolabeling in the CA1 subregion of the hippocampus (left) and C3 immunolabeling of entire hemispheres (right) in 18-month-old AppSAA +/+ and AppSAA KI/KI mice. d Quantification of GFAP immunoreactivity in the CA1, CA3, dentate gyrus (DG), and neocortex (CTX). e Quantification of GLT-1 immunoreactivity in the CA1, CA3, DG, and CTX. f Quantification of astrocytic C3 immunoreactivity in the CA1, CA3, DG and CTX. Scale bars: 300 μm for hemisphere images and 100 μm for all other images. Graphs show means ± SEM. Mann-Whitney test, *P < 0.05, **P < 0.01 versus AppSAA +/+; n = 5 AppSAA +/+, 7 AppSAA KI/KI.