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. 2017 Apr 12;37(15):4023–4031. doi: 10.1523/JNEUROSCI.3442-16.2017

Figure 6.

Figure 6.

LRP1 deficiency in astrocytes leads to an increase in neuroinflammation. A–C, Brain sections from APP/PS1 and APP/PS1; aLrp1−/− mice (n = 8 or 9/group) at 12 months of age were immunostained for the astrocyte marker GFAP (A) and quantified (C). Scale bar, 1 mm. B, Higher-magnification images for GFAP immunostaining in the cortex and hippocampus. Scale bar, 200 μm. Data are mean ± SEM. *p < 0.05. D–F, Brain sections from APP/PS1 and APP/PS1; aLrp1−/− mice (n = 8 or 9/group) were immunostained for the microglia marker Iba1 (D) and quantified (F). Scale bar, 1 mm. E, Higher-magnification images for Iba1 immunostaining in the cortex and hippocampus. Scale bar, 200 μm. Data are mean ± SEM. *p < 0.05 (two-tailed Student's t test). **p < 0.01 (two-tailed Student's t test). G, GFAP in the cortex (n = 9/group) of APP/PS1 and APP/PS1; aLrp1−/− mice examined by Western blotting. Data are mean ± SEM. *p < 0.05. H, GFAP in the cortex (n = 8 or 9/group) of control and aLrp1−/− mice (in the absence of APP/PS1 background) examined by Western blotting. Data are mean ± SEM. I, TNF-α and interleukin-1β (IL-1β) in the cortex of APP/PS1 and APP/PS1; aLrp1−/− mice (n = 9/group) evaluated by real-time PCR. Data are mean ± SEM. *p < 0.05 (two-tailed Student's t test).