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. 2019 Dec 4;19(2):e13078. doi: 10.1111/acel.13078

Figure 6.

Figure 6

Deletion of REV‐ERBα mitigates amyloid plaque deposition in 5XFAD mice. (a) Representative image from thioflavin‐S staining of the brain sections including the cortex, hippocampus, and thalamus from 5XFAD and 5XFAD/REV‐ERα knockout (RKO) mice at 3.5 months. (n = 6–7 mice were analyzed per group). (b) Western blot analysis of Aβ peptide (4KDa) and β‐actin expression in each brain lysate. β‐actin was used as a loading control. **p < .01, ***p < .001 compared to the 5XFAD. (c) Representative image of X34 staining in the brain of 5XFAD and 5XFAD/RKO. (d) Quantification of X34‐positive plaque number and % area of X34 staining for each group mice brain using Image J. *p < .05, **p < .01 compared to the 5XFAD. (e) Representative images from confocal analysis of IBA1 and CD68 staining surrounding X34‐positive plaques in the cortex of 5XFAD and 5XFAD/RKO (X34 in Blue, IBA1 in Red, and CD68 in Green) (f) Quantification of X34‐positive plaque and plaque‐associated microglia (Iba1)/phagocytic microglia (CD68). Total volume of Iba1 and CD68 were normalized by X34 volume for each plaque. **p < .01 compared to the 5XFAD (n = 30–44 plaques) (g) mRNA expression of Iba1 and CD68 in the cortex of each group mice (WT, RKO, 5XFAD, 5XFAD/RKO). *p < .05, **p < .01, and ***p < .001