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Figure 2 | Molecular Neurodegeneration

Figure 2

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

Figure 2

Extended T0 treatment increases the levels of soluble apoE and apoA-I proteins and decreases insoluble Aβ in APP23 mice. APP23 mice (n = 5) were treated by gastric gavage with T0 for 4 weeks at a dose of 20 mg/kg/day and age-matched control mice (n = 5) received vehicle. At the end of the treatment one hemisphere was used for total RNA isolation and the other was used for protein extraction. Soluble brain proteins were extracted with DEA followed by the extraction of the insoluble proteins from the pellet using formic acid. A: Expression level of ABCA1, apoE and apoA-I mRNA as determined by RT-QPCR. B: Insoluble Aβtotal in aliquots from the insoluble brain fraction was determined by WB using by 6E10 antibody which recognizes both Aβ40 and Aβ42. The level of Aβtotal was normalized to the level of APP full length (APPfl). C: Amounts of soluble apoE and apoA-I were determined by WB of formic acid extracted brain homogenates. The bands were quantified and the level of apoE normalized to the level of GAPDH. D: Insoluble apoE and apoA-I were determined by WB of formic acid extracted brain homogenate as in C. Values (A, B, C and D) are means ± SEM and represent fold of vehicle (two-tailed Student's t test). E. The level of insoluble Aβtotal correlates negatively to the level of soluble apoE (Spearman Nonparametric correlation analysis).

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