Fig. 6From: Unconjugated PLGA nanoparticles attenuate temperature-dependent β-amyloid aggregation and protect neurons against toxicity: implications for Alzheimer’s disease pathologyPLGA alters the lag phase of Aβ1–42 aggregation kinetics at different temperatures. ThT kinetic assay showing aggregation of 10 µM Aβ1–42 in the absence and presence of 5–25 µM of PLGA over 5 h incubation (lag phase) at 27 °C (A), 37 °C (B) and 40 °C (C). Note the decreased duration of the lag phase with rise in temperature in the absence and presence of presence of PLGA. STEM images of 10 µM Aβ1–42 in the absence (D–F) and presence of 25 µM PLGA (G–I) after 5 h incubation at 27 °C (D, G), 37 °C (E, H) and 40 °C (F, I). Note the attenuation of Aβ fibril formation in the presence of PLGA nanoparticles. DLS analysis revealing diameter (J–L) and average size (M–O) of 10 µM Aβ1–42 in the absence and presence of 25 µM PLGA after 5 h incubation at 27 °C (J, M), 37 °C (K, N) and 40 °C (L, O). Note the attenuation of Aβ aggregation at different temperatures as a function of PLGA concentrations. PLGA nanoparticles are highlighed with arrowsBack to article page