Figure 1

Inhibition of the proteasome or autophagy partially affects Aβ1-42 and p-Tau clearance. To dissect out the contribution of the proteasome from autophagy-lysosome in amyloid clearance, primary hippocampal neurons (DIV14) were infected with lentivirus plasmids, and then treated with 1 μl DMSO or autophagy modulators (Nilotinib or Bafilomycin-A1) and/or proteasome inhibitor (MG132). Histograms represent ELISA concentrations of A) Aβ1-42 and time course showing the distribution of intracellular and media B) Aβ1-42 and C) p-Tau Ser 396. D) p-Tau Ser 396 in the presence of modulators of autophagy and the proteasome. Insert). WB analysis on 4-12% NuPAGE SDS gel showing expression of the lentiviral tag V5, Aβ1-42, human Tau (HT7) and total Tau relative to actin. E) WB analysis on 10% NuPAGE SDS gel showing AT8 levels relative to actin. F) Histograms represent 20S proteasome activity assay in human M17 neuroblastoma cells. G) RT-PCR showing the effects of Nilotinib on lentiviral gene expression relative to GAPDH. # indicates significantly different to LacZ, Asterisk is significantly different to Aβ1-42 + DMSO or as indicated, bars are mean ± SEM, two-way ANOVA.