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. Author manuscript; available in PMC: 2015 Dec 1.

Published in final edited form as: Neuromolecular Med. 2014 Dec;16(4):686–696. doi: 10.1007/s12017-014-8318-6

Fig. 3 — Expression of (A) LRP1 and (B) LDLR in cerebrovasculature isolated from apoE transgenic mice. Human Aβ(1–42) or vehicle was intracranially administered to male mice (4–6 months old). Ten minutes after the intracerebral injection, the brains were collected and various brain fractions were isolated. LRP1 or LDLR levels in the cerebrovasculature were determined using an ELISA and normalized to total protein content using the BCA protein assay. Values represent mean ± SEM (n = 6 animals) and are expressed as ng of LRP1 or LDLR per mg protein. No comparisons reached statistical significance as determined by ANOVA and Bonferroni post-hoc test.

Fig. 3 — Expression of (A) LRP1 and (B) LDLR in cerebrovasculature isolated from apoE transgenic mice. Human Aβ(1–42) or vehicle was intracranially administered to male mice (4–6 months old). Ten minutes after the intracerebral injection, the brains were collected and various brain fractions were isolated. LRP1 or LDLR levels in the cerebrovasculature were determined using an ELISA and normalized to total protein content using the BCA protein assay. Values represent mean ± SEM (n = 6 animals) and are expressed as ng of LRP1 or LDLR per mg protein. No comparisons reached statistical significance as determined by ANOVA and Bonferroni post-hoc test.