Figure 3.

CTEP treatment for 24, but not 36, weeks reduced Aβ pathology in APPswe/PS1ΔE9 mice. Representative images of Aβ staining and quantification of plaque density in cortical and hippocampal brain slices from age-matched APPswe/PS1ΔE9 (APP) mice following treatment with either vehicle or CTEP (2 mg/kg) for (A) 24 or (B) 36 weeks. Images are representative of four independent experiments (scale bar, 50 μm). Data represent mean ± SD following the quantitation of five different 900 μm² regions in the cortex and two different 900 μm² regions in the hippocampus from six brain slices in four independent mice for each group. *P < 0.05 versus the same region of vehicle-treated age-matched APP mice. Statistical significance was assessed by unpaired Student’s t test. (C) Mean ± SD of the whole-brain Aβ oligomer concentrations (pg/mg protein) in age-matched wt and APP mice after either a 24 week or 36 week treatment with either vehicle or CTEP (n = 4–5). The asterisk (∗) denotes significant difference at P < 0.05. (D) Representative Western blots and quantification of folds change in Amyloid precursor protein with the corresponding β-tubulin loading control from age-matched wt and APP mice after either a 24 week or 36 week treatment with either vehicle or CTEP (n = 4). Values represent mean ± SD and were expressed as a fraction of the 24 week, vehicle-treated wt value. *P < 0.05 versus 24 week, vehicle-treated wt mice. Statistical significance for panels C and D was assessed by two-way ANOVA and Fisher’s LSD comparisons.