Fig. 6

CS treatment of EFAD mice at ages of high pathology does not impact AD-like phenotype to a great extent. A Study design. EFAD mice were treated with CS or VC by daily intraperitoneal injections (i.p.) from 8 to 10 months of age. B There were no differences in % of survival due to treatment (p = 0.8422), or APOE genotype (P = 0.7353), however males survived less compared to females (p < 0.0069). C CS treatment did not affect body weight. D Liver weights were reduced by CS treatment in female mice (E3FADs, p < 0.0001; E4FADs, p = 0.0227). E–H CS treatment did not modulate soluble or detergent-soluble apoE. F and H CS treatment decreased insoluble apoE in female EFAD mice (E3FAD, p < 0.0472; E4FAD, p = 0.0291). I There were no effects of CS treatment on ABCA1 levels. J Representative images of Aβ immunostaining (MOAB-2) in sagittal sections. Scale bar: 100 μm. K CS reduced % area covered by Aβ in male E4FAD (p = 0.0005). L Soluble oAβ levels were not affected by CS treatment except for a non-significant trend in male E4FAD mice (p = 0.077). M Insoluble Aβ levels were not affected by CS treatment except for a non-significant trend in male E4FAD mice (p = 0.072). Acquisition (N) and probe (O) trials in the Morris water maze (MWM) test. In the acquisition phase, there was an effect of day but not treatment in all groups. O Probe/memory trial performance. There was a reduction in platform crosses with CS treatment in male E4FAD (p = 0.0064). P CS treatment did not affect drebrin levels. Data are expressed as mean ± SEM for behavior, body weights, and biochemical measures (n = 9–12); and IHC and western blot (n = 6–8). MWM acquisition data were analyzed by repeated measures using 4-way ANOVA, followed by Tukey’s post hoc. % survival was analyzed by chi-square (Mantel-Cox) test. The rest of the data was analyzed by t-test. All data is from the same cohort of mice; the n’s differ because of study design, technical issues, and outlier tests