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. 2013 Dec 4;33(49):19276–19283. doi: 10.1523/JNEUROSCI.3487-13.2013

Figure 2.

Figure 2.

LRP1 deletion in neurons exacerbates Aβ deposition in the cortex of APP/PS1 mice. A, Cortex from control APP/PS1 and APP/PS1; Lrp1−/− mice were costained with an LRP1 antibody and a neuronal marker NeuN or an astrocyte marker GFAP at 12 months of age. Scale bar, 50 μm. B, LRP1 expression in cortex from APP/PS1 and APP/PS1; Lrp1−/− mice was detected by Western blot at 6–7 (n = 4–5), 12–13 (n = 6–7), and 18–20 months (n = 5–6) of age. C, The concentrations of insoluble Aβ40 and Aβ42 levels in the cortex extracted in guanidine (GDN) from control APP/PS1 and APP/PS1; Lrp1−/− mice were analyzed by ELISA at 6–7 (n = 4–5), 12–13 (n = 6–7), and 18–20 months (n = 5–6) of age. D, Aβ plaques in brain sections from control APP/PS1 and APP/PS1; Lrp1−/− mice (12–13 months of age) were immunostained with a pan-Aβ antibody. Scale bar, 1 mm. E, Amyloid plaque burdens in the cortex from control APP/PS1 and APP/PS1; Lrp1−/− mice were quantified after scanning Aβ immunostaining by the Positive Pixel Count program (Aperio Technologies) at 12–13 months of age (n = 6–7). F, G, The concentrations of soluble Aβ40 and Aβ42 levels in the cortex extracted in TBS (F) and TBS-TX (G) from control APP/PS1 and APP/PS1; Lrp1−/− mice were analyzed by ELISA at 12–13 (n = 6–7) and 18–20 months (n = 5–6) of age. H, I, LRP1 expression in cerebellum from APP/PS1 and APP/PS1; Lrp1−/− mice was detected by Western blot at 12–13 months (n = 4), and the concentrations of insoluble Aβ40 and Aβ42 levels in the cortex extracted in GDN were analyzed (I). Data were plotted as mean ± SEM *p < 0.05; **p < 0.01. N.S., Not significant.