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. Author manuscript; available in PMC: 2019 Jul 7.
Published in final edited form as: Nat Neurosci. 2019 Jan 7;22(2):191–204. doi: 10.1038/s41593-018-0296-9

Figure 2. Reduced microglial clustering, CD68 and Trem2 expression in microglia around newly seeded plaques in Trem2 loss of function mice.

Figure 2.

(a) First panel: Random distribution of IBA1-positive microglia in C57BL6 mice. Second panel: Clustering of IBA1 and Trem2-positive microglia around seeded plaques in the hippocampus of APPPS1/Trem2+/+. Third and fourth panel: Loss of Trem2 function reduces microglia clustering around seeded plaques. (b) IBA1-positive microglia clustering around seeded amyloid plaques (n+/+=9 mice, n−/−=7 mice, np.T66M=7 mice, F2,20=38.87, p=1.5E-7) normalized to seeded amyloid pathology shown in Fig. 1c. (c) IBA1 immunoreactivity quantified in the hippocampus excluding seeded dentate gyrus (n+/+=10 mice, n−/−=9 mice, np.T66M=9 mice, F2,25=1.657, p=0.2109) (d) First panel: CD68 expression is at the detection limit in C57BL6 mice. Second panel: Increased CD68 staining in IBA1-positive microglia around seeded plaques in the presence of functional Trem2. Third and fourth panel: reduced CD68 expression in microglia around seeded plaques in the absence of functional Trem2. (e) Quantification of CD68-positive microglia in the seeded dentate gyrus (n=6 mice/genotype, F2,15=44.87, p=4.6E-7) normalized to seeded amyloid pathology shown in Fig. 1a. Dotted white boxes indicate the area in each staining that is merged and shown at higher magnification. Data represent mean ± SEM. One-way ANOVA, Dunnett’s post hoc analysis; n.s. p>0.05; ***p<0.0005.