Figure 13

Reduction of brain plaque load in younger (a–h) and older (i–j) TASD-41 APP transgenic mice by proanthocyanidin B2 (compound h2). (a–h) Reduction of brain Aβ 1–42 and Aβ 1–40 load by proanthocyanidin B2 (i.e. compound h2) in younger (4 months old at start; 7 months old at sacrifice) APP transgenic mice. n = 10 per group. (a) Proanthocyanidin B2 caused a significant (p < 0.05) 18.5% reduction of insoluble Aβ 1–42, and (c) a significant (p < 0.05) 70.4% reduction of soluble Aβ 1–42, as determined by Aβ ELISAs. (b) Compound h2 also caused a significant 23.9% reduction of insoluble Aβ 1–40, and (d) a significant 58.9% reduction in soluble Aβ 1–40 in brains of TASD-41 transgenic mice. n = 4 per group. (e–h) Reduction of brain amyloid load and plaque number by proanthocyanidin B2 in younger (4 months old at start; 7 months old at sacrifice) TASD-41 transgenic mice. n = 10 per group. (e) Image analysis of Thioflavin-S stained sections from cortex revealed that proanthocyanidin B2 (h2 treatment) caused a significant 74.2% reduction in Thioflavin S amyloid load, and (f) a significant 74.9% reduction in plaque number (per sq. mm). Similarly, Congo red staining revealed a significant 82.9% in % amyloid load (g), and an 80.8% reduction in plaque number (h). Thioflavin S-stained sections from cortex of older TASD-41 APP transgenic mice (6 months old at start; 9 month old at sacrifice) revealed that proanthocyanidin B2 caused a significant 58.2% reduction in Thioflavin S amyloid load (i), and a significant 51.9% reduction in plaque number (j). *p < 0.05, **p < 0.01, ***p < 0.001, by Student’s t-test. Bars represent mean +/− SEM.