Figure 4
Attenuation of tau aggregation by PLGA. (A–C) PLGA (20 µM) attenuates aggregation of 10 µM 0N4R tau in presence of heparin without Aβ1-42 seed as revealed by ThT kinetic assays (A) and respective fluorescence (B) as well as STEM (C) images over 40 h incubation. The fluorescence (B) and STEM (C) images showed the relative decrease in the amount of tau fibrils in presence of 20 µM PLGA. (D,E) DLS analysis of 10 µM 0N4R tau + heparin ± PLGA without Aβ1-42 seeds revealed a differential decrease in the diameter of tau in the presence of PLGA compared to control tau as depicted by size distribution curves (D) and and histogram (E) representing average aggregate size (left side Y axis) and mean peaks of tau aggregates for a given condition (right side Y axis). (F–J) Native PLGA (20 µM) attenuates Aβ1-42 seed-induced aggregation of 10 µM 1N3R tau in the presence of heparin as revealed by ThT kinetic assays (F) and respective fluorescence (G) as well as STEM (H) images over 40 h incubation. The fluorescence (G) and STEM (H) images showed the relative decrease in the amount of tau fibrils in presence of 20 µM PLGA. (I,J) DLS analysis of Aβ1-42 seed-induced 10 µM 1N3R tau reveals a differential decrease in the diameter of tau in the presence of PLGA compared to control tau as depicted by size distribution curves (I) and and histogram (J) representing average aggregate size (left side Y axis) and mean peaks of tau aggregates for a given condition (right side Y axis). All ThT kinetic graphs represented average mean ± SEM of three separate experiments, each performed with six replicates for each condition.
