Fig. 7From: Myeloid deficiency of the intrinsic clock protein BMAL1 accelerates cognitive aging by disrupting microglial synaptic pruningMicroglial gene expression changes in young and aged WT and Bmal1 cKO mice. A Principal component analysis (PCA) shows distinct clustering of young CD11bcre and CD11bcre;Bmal1lox/lox (n = 6/group) mice versus aged CD11bcre (n = 6) and CD11bcre;Bmal1lox/lox (n = 7) mice. B Venn diagram of number of differentially expressed genes in young and aged CD11bcre;Bmal1lox/lox mice. C Volcano plot of -log10 p-adjusted value versus −log2 fold change of normalized counts between aged CD11bcre and CD11bcre;Bmal1lox/lox mice. Each dot represents a single transcript. Cyan dots denote significantly differentially expressed genes. Orange dots denote genes that are unchanged between the genotypes (adjusted p-value < 0.05)Back to article page