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Fig. 6 | Acta Neuropathologica Communications

Fig. 6

From: Absence of Apolipoprotein E is associated with exacerbation of prion pathology and promotes microglial neurodegenerative phenotype

Fig. 6

Exaggerated microglia activation in prion infected Apoe−/− mice. a and c Representative microphotographs of coronal cross-sections through the VPN thalamic nucleus and the S1 primary somatosensory cortex immunostained against Iba1 from indicated animal groups, respectively. b and d Quantitative analysis of Iba1+ load in the VPN and the S1 cortex, respectively (n = 8–12 mice/group). e Representative microphotographs of Iba1/DAPI double stained microglia in the layer V of the S1 cortex. f Enumeration of Iba1+/DAPI+ microglia in the layer V of the S1 cortex (n = 6–8 mice/group). g and i Representative microphotographs of coronal cross-sections through the VPN and the S1 cortex immunostained against CD68 from indicated animal groups, respectively. h and j Quantitative analysis of CD68+ load in the VPN and the S1 cortex, respectively (n = 8–12 mice/group). While the Iba1+ load and the number of microglia increases earlier in the course of prion infection and is more robust in 22L Apoe−/− mice compared to 22L WT mice, the CD68+ load is comparable between the genotypes at 15 wpi, while at 23 wpi it is lower in 22L Apoe−/− mice compared to 22L WT mice. b, d, f, h, j p < 0.0001 (ANOVA); **p < 0.01, ***p < 0.001, and ****p < 0.0001 (Holm’s-Sidak’s post hoc test). All numerical values represent mean + SEM. Scale bars: 50 μm in a, e, and g, and 100 μm in c and i

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