Fig. 4.

EGCG remodels Aβ₄₂ fibrils and oligomers into benign SDS-resistant structures. (A) Fibrillar Aβ₄₂ (15 μM) was incubated with EGCG (15 μM) for up to 24 h in PBS at 37 °C. EGCG-induced remodeling of Aβ₄₂ fibrils into spherical assemblies was monitored by atomic force microscopy. (B) Fibrillar Aβ₄₂ (equivalent 15 μM monomer) was incubated in the absence (Black) or presence of EGCG (15 μM, Blue; 75 μM Red) in PBS at 37 °C. Loss of ThT fluorescence was monitored at time intervals of 10 min, preceded by 5 s shaking each. (C) Immunofluorescence microscopy shows loss of intracellular Aβ aggregates (Green) in 7PA2 cells after ECGG (10 μM) treatment for 3 d. (phalloidin, Red; DAPI, Blue). (D) LDH release in 7PA2 cells after introduction of Aβ₄₂ aggregates. The assay was performed as described in Fig. 3B. Values represent means ± SD, n = 8; *** P < 0.0005. (E) Aβ₄₂ aggregates (15 μM) were incubated with the indicated amounts of EGCG for 24 h at 37 °C. Aggregates were then were diluted into the cell culture media at the indicated concentrations and added to PC12 cells. Metabolic activity was monitored after 3 d by MTT reduction. Values represent means ± SD (n = 3) normalized to cells neither treated with Aβ nor with EGCG; * P < 0.01, ** P < 0.001.