Figure 2.
Chronic treatment of Tg2576 mice with GSPE prevents amyloid neuropathology by prevention of Aβ oligomerization. A, B, GSPE has no effect on body weight (A) or liquid consumption (B) in Tg2576 mice after 5 months of treatment. C, Assessments of PBS-soluble, extracellular HMW Aβ peptide content in the brain using an antibody (A11) specific for HMW oligomeric Aβ peptides in a dot blot analysis. C, Inset, Representative dot blot analysis of HMW soluble Aβ contents. D, Western blot analysis of soluble extracellular HMW oligomeric Aβ peptide (antibody A11) and monomeric Aβ peptide (antibody 6E10) in the brain of Tg2576 mice. E, Assessment of Aβ1–42 and Aβ1–40 peptide concentrations in the brain of GSPE-treated or control mice. F, Stereological assessment of cerebral cortex and hippocampal formation Aβ amyloid plaque burden in GSPE-treated or control mice expressed as thioflavin-S-positive volume as a percentage of regional volume. F, Inset, Representative photographs of thioflavin-S-positive Aβ amyloid plaque neuropathology in neocortex (CTX) and hippocampal formation (Hippo) in untreated control (top) and GSPE-treated (bottom) Tg2576 mice. Values represent group mean ± SEM. n = 5–8 mice per group. *p < 0.05, **p < 0.01 by two-tailed Student's t test analysis. CTL, Control.