Fig. 8

Effects of β1 antibody treatment in APP23 mice. Schematic representation of anti-Aβ (β1) treatment effects when applied before the onset of neurodegeneration and Aβ plaque deposition (3–5 months) and when provided with prevalent pathology (7–11 months). Anti-Aβ antibody treatment protected type 1 commissural neurons (Type 1) from dendritic degeneration accumulated antibody-bound oligomers, fibrils and protofibrils in the soluble fraction containing Aβ. These effects were seen in B-Aβ stage 1. No positive effect on Type 1 commissural neurons was found when β1-treatment was performed from 7 to 11 months of age. Moreover, plaque loads and biochemically detectable amounts of soluble, dispersible, membrane-associated, and plaque-associated Aβ were similar in β1- and PBS-treated APP23 mice. Aβ aggregation at 11 months of age corresponded to B-Aβ stage 3, i.e. fully mature, AD-related Aβ aggregates. Here, β1-treatment caused epitope modifications of Aβ aggregates resulting in less β1- and B10AP-positive plaques in treated mice. Moreover, at 11 months of age presence of antibody-bound non-modified Aβ in the serum was visible, whereas antibody-bound modified Aβ_N3pE and pAβ were not seen in the blood plasma