Expression profiling in APP23 mouse brain: inhibition of Aβ amyloidosis and inflammation in response to LXR agonist treatment-2

<p><b>Copyright information:</b></p><p>Taken from "Expression profiling in APP23 mouse brain: inhibition of Aβ amyloidosis and inflammation in response to LXR agonist treatment"</p><p>http://www.molecularneurodegeneration.com/content/2/1/20</p><p>Molecular Neurodegeneration 2007;2():20-20.</p><p>Published online 22 Oct 2007</p><p>PMCID:PMC2214725.</p><p></p>mpi and mRNA expression of ABCA1, apoE and ABCG1 were determined by RT-QPCR; h-v, (black bars) – vehicle treatment, hippocampi; h-T0, (white bars) – T0 treatment, hippocampi, c-v (grey bars), vehicle treatment, cortex; c-T0 (hatched bars), T0 treatment, cortex. Primary neurons, astrocytes and microglia were established from wild type (wt) and LXRαβdouble knockout mice (dko). Cells were treated with 10 μM T0 for 24 hours and mRNA expression of ABCA1 () and apoE () measured by RT-QPCR. Values are means ± SEM and represent fold of vehicle for the corresponding genotype. : ABCA1 protein level in wild type (wt) and LXRαβ(dko) neurons was determined by WB. The level of ABCA1 was normalized to the level of GAPDH, and presented (means ± SEM) as fold of vehicle of the corresponding genotype in the graph bellow