Figure 3.
Aβ-GFP Tg mice do not exhibit the extracellular deposition of Aβ but increased phosphorylated tau. (A,B) Anti-Aβ (6E10) immunostaining of brain sections of 24-month-old non-Tg (A) and Aβ-GFP Tg mice (B). Insets in (A) and (B) show the magnification of the boxed areas of the hippocampal CA1 pyramidal cell layer. Although the pyramidal cells of hippocampus CA1 regions were immunopositive in Aβ-GFP Tg mice (inset in B), no extracellular amyloid depositions were observed in any regions we examined. No immunoreactivity was observed in non-Tg littermates (A). Scale bars; 500 μm (A,B), 250 μm (insets). (C) Representative immunoblots showing the expression of phosphorylated tau (p-tau) in hippocampal homogenates (3- and 18-month-old: 30 μg/lane each) in non-Tg (lanes 1, 3) and Aβ-GFP Tg (lanes 2, 4). Immunoblotting of actin served as loading control and band intensities were normalized by it. Histograms represent the ratios of phosphorylated tau in Aβ-GFP Tg against non-Tg mice. No significant difference was observed between Aβ-GFP Tg and non-Tg mice in young age but tau phosphorylation was increased significantly in Aβ-GFP Tg mice at 18-month-old (*p < 0.05, Mann-Whitney’s U test, n = 8 (3 M) and 8 (18 M) animals each, data are presented as means ± SEM).