Figure 3

Boosting autophagy leads to Aβ1-42 clearance in WT but not Tau^−/−mice. WT and Tau^−/− mice were injected with lentiviral Tau ± Aβ1-42 for 3 weeks and treated I.P. with 10 mg/kg Nilotinib or DMSO once a day for 3 weeks. Brain tissues were fractionated to isolate AVs and human specific ELISA was performed. Histograms represent concentration of A) Aβ1-42, insert is WB on 4-12% SDS NuPAGE gel showing LC3 and LAMP-2a as AV markers, B) Aβ1-42 in AV20, and C) Aβ1-42 in lysosomal fractions in WT and Tau^−/− mice. ELISA concentrations of Ser 396 Tau in D) AV10, E) AV20, and F) lysosomal fractions in WT and Tau^−/− mice. WB analysis on 4-12% SDS NuPAGE gel of total brain extracts from WT mice showing G) V5 to verify equal expression of all lentiviruses, human Tau (HT7), total Tau, AT8 and AT180 relative to actin. H) shows p-Tau Ser 262, Ser 396 and autophagic markers Beclin-1 and LC3-I/II relative to actin. WB analysis on 4-12% SDS NuPAGE gel of total brain extracts from Tau^−/− mice showing I) V5, human Tau (HT7), total Tau, AT8, and AT180 relative to tubulin. J) shows p-Tau Ser 262, Ser 396 and autophagic markers Beclin-1, LC3-I and LC3-II relative to actin. Asterisk indicates significantly different to Aβ1-42 + DMSO, bars are mean ± SEM, two-way ANOVA.