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. Author manuscript; available in PMC: 2015 Mar 3.
Published in final edited form as: J Alzheimers Dis. 2014;41(2):535–549. doi: 10.3233/JAD-132789

Figure 4. LXR treatment increases Abca1 and ApoE lipidation in the brain of treated mice.

Figure 4

A, Abca1 level was measure by WB of RIPA extracts from cortex and hippocampus of treated mice. N=6 mice per group. Analysis is by one-way ANOVA, p < 0.01, Dunnett’s post-test **, p < 0.01 versus control IgG. B, ApoE level was measured in soluble extract of cortex and hippocampus by ELISA as described in the methods. N=4–14 mice per group. One-way ANOVA, p < 0.001, Dunnett’s post-test **, p < 0.01 and *, p < 0.05 versus control IgG. C, CTFα/β were measured on WB in RIPA extracts from cortex and hippocampus of treated mice. Analysis is by one-way ANOVA shows no significance, N=6 mice per group. D, Shown are representative pictures for Abca1 and CTFα/β WB. N.S. is non-specific band. E, Native gel electrophoresis demonstrated an increase of ApoE lipidation in TBS soluble brain extract. Native standards are shown on the left. ApoEko brain extract is shown as negative control.