Fig. 3
07/2a IgG2a and 3A1 IgG1 mAb’s lowered guanidine-HCl-extracted Aβ in aged APPSWE/PS1ΔE9 mice. Significant decreases in guanidine-HCl-extracted pGlu-3 Aβ (p < 0.05), Aβx-42 (p < 0.01), Aβx-40 (p < 0.05), and Aβx-38 (p < 0.05) were observed in Tg mice treated with 07/2a IgG2a mAb compared to PBS-treated Tg mice (a–d). Similarly, treatment with 3A1 mAb reduced guanidine-HCl-extracted Aβx-42 (p < 0.01), Aβx-40 (p < 0.05, t-test), and Aβx-38 (p < 0.05, t-test) in Tg mice compared to PBS controls (b–d). Treatment of the Tg mice with 3A1 IgG1 mAb resulted in a significant increase in plasma levels of Aβx-42 (0.01), Aβx-40 (p < 0.001), and Aβx-38 (p < 0.001) with no differences observed in Tg mice treated with anti-pGlu-3 Aβ mAbs, 07/1 IgG1 or 07/2a IgG2a, compared to PBS-treated Tg mice (e–g). No significant (N.S) differences in hemosiderin-positive staining were observed between antibody-treated Tg mice versus PBS-injected Tg mice or WT mice (h). n = 13–15 per group. All data, excluding baseline, are expressed as the mean ± SEM. ANOVA with Neuman-Keuls post test: ***p < 0.001, **p < 0.01, and *p < 0.05 versus Tg PBS. Student’s t-test: #p < 0.05