Tau deletion impairs autophagic clearance. Primary hippocampal neurons from WT and Tau−/− mice 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 soluble and insoluble brain extracts of A) human Aβ1-42 and B) p-Tau Ser 396. WT (C57BL/6) and Tau−/− mice were injected with 1×106 multiplicity of infection (MOI) of lentiviral human Tau, Aβ1-42, Tau ± Aβ1-42 and adjusted with LacZ. All animals were treated 3 weeks post-injection with daily 10 mg/kg IP injection or 30 μL DMSO once a day for 3 (additional) consecutive weeks. Histograms represent ELISA concentrations of total brain extracts of C) human Aβ1-42 and D) p-Tau Ser 396. Asterisk is significantly different to Aβ1-42 + DMSO or as indicated, # indicates significantly different to Aβ1-42 + DMSO in WT mice. Bars are mean ± SEM, two-way ANOVA.