Fig. 6
Myelin sulfatide deficiency induced AD-like neuroinflammation even in the absence of ApoE. (A,B) Representative immunofluorescence images from brain of 3-mo-old ApoE+/+/CST+/+, ApoE−/−/CST+/+, and ApoE−/−/CST−/− mice using antibodies against GFAP (red) and Iba1 (green). Cx: cortex; CC: corpus callosum; CA1: Cornu Ammonis 1 region of the hippocampus. Scale bar: 200 μm. (C-F) The brain mRNA from the four genotypes (ApoE+/+/CST+/+, ApoE−/−/CST+/+, ApoE+/+/CST−/−and ApoE−/−/CST−/−) was accessed using NanoString neuroinflammation panel. (C) Volcano plot displaying -log10 p-value and log2 fold change for each gene to show the CST KO effect (middle) and the ApoE KO effect in the presence (CST+/+, left) or absence of sulfatide (CST−/−, right). (D) Venn diagrams showing the number of specific and shared upregulated DEGs from ApoE−/− vs. WT, CST−/− vs. WT and the DEGs listed in Fig. 3C. The gene lists were shown in Fig. S9. (E) Venn diagrams showing the number of specific and shared upregulated DEGs from CST−/− vs.WT, ApoE−/−/CST−/− vs. CST−/− and the DEGs listed in Fig. 3C. The gene lists were shown in Fig. S9. (F) Linear counts of several typical microgliosis- and astrogliosis-related genes in ApoE+/+/CST+/+, ApoE−/−/CST+/+, ApoE+/+/CST−/−and ApoE−/−/CST−/− mouse brain. Heteroscedastic Welch’s t-Test, n = 3. *p < 0.05, ns: no statistical significance