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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Myeloid deficiency of the intrinsic clock protein BMAL1 accelerates cognitive aging by disrupting microglial synaptic pruning

Fig. 6

Myeloid Bmal1 deletion increases microglial activation but decreases lysosomal function in aged mice. A Representative confocal images of IBA1 (green) and CD68 (red) expression in the hippocampal CA1 region of aged CD11bcre and CD11bcre;Bmal1lox/lox mice (18–20 months, n = 6/group). Scale bar, 50 µm. White dotted lines in A indicate region of interest quantified in C. B Higher magnification of microglia in CA1 hippocampal region from aged CD11bcre and CD11bcre;Bmal1lox/lox mice.Scale bar, 5 µm. C Mean fluorescence intensity of IBA1, CD68, proportion of IBA1-positive ( +) cells that are CD68 + , and the number of DAPI + IBA1 + microglia (n = 6/group). D Representative immunoblot of IBA1 in aged CD11bcre and CD11bcre;Bmal1lox/lox mice (18–20 months; n = 6/group). E Quantification of IBA1 immunoblot normalized to ß-actin. F Representative images of skeletonized microglia overlaid on original image from aged CD11bcre and CD11bcre;Bmal1lox/lox mice. G Quantification of microglial complexity. Scale bar, 5 µm. Every measurement that contained ≤ 2 endpoints with a maximum branch length of less than the cutoff value of 0.5 µm was removed from the analysis. Data are represented as the mean ± SEM. P-values were calculated using two-tailed Student’s t-test

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