Skip to main content
. 2012 Jul 25;32(30):10117–10128. doi: 10.1523/JNEUROSCI.5268-11.2012

Figure 3.

Figure 3.

PPARγ activation drives the expression of LXR target genes in vivo. Six (A, C)- and 12 (B, D)-month-old APP/PS1 mice were gavaged orally with 80 mg · kg−1 · d−1 pioglitazone (Pio) or vehicle (H2O) for 9 d. Cortical homogenates were then analyzed by Western blot for levels of abca1, apoe, and actin (A, B) and quantified (C, D). (mean ± SEM, *p < 0.05, **p < 0.01, n ≥ 6 animals/treatment). Quantitative PCR results for LXR target genes from cortices of 6 (E)- or 12 (F)-month-old APP/PS1 animals treated with pioglitazone (Pio) or vehicle (Veh) or wild-type animals treated with vehicle (WT) for 9 d (mean ± SEM, Student's t test, *p < 0.05, **p < 0.01, n ≤ 13 animals/group). Fold change is reported as a percentage of vehicle-treated WT animals.