Disease Modifying Therapies for Alzheimer's Disease Targeting Aβ Oligomers: Implications for Therapeutic Mechanisms
Figure 1
Antifibrillogenic activities of 72D9. (a) Fibril formation of A1-42 at 12.5 μM was assayed on the basis of ThT fluorescence intensity at 37°C for 24 h: dose-dependent inhibition of A1-42 assembly was observed for 72D9; however, nonspecific IgG2b failed to inhibit seed-free A1-42 (540,000 ThT-negative supernatants) assembly. (b) Electron micrographs of incubation mixture containing 50 μM A1-42 preincubated with IgG2b or 72D9. A1-42 with control IgG2b shows mature fibrils (left panel). A1-42 with 72D9 shows nonfibrillar amorphous structures (right panel). Scale bar = 200 nm. Experimental results were analyzed with one-way ANOVA, followed by the Tukey test for post hoc analysis: statistical significance compared with A1-42 alone ().
