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. 2020 Sep 23;15(9):e0239584. doi: 10.1371/journal.pone.0239584

Fig 3. Induction of tau phosphorylation and tau-dependent cell death by wt and E22G Aβ but not E22Δ Aβ.

Fig 3

A: Cytotoxicity in human tau expressing slices from Tg2576, arcAβ- and E22ΔAβ tg mice and the respective non-transgenic littermates, measured with CytotoxGlo assay. Increased cell death was observed in Tg2576 and arcAβ tg slices, although not significant in arcAβ tg slices, but not in E22ΔAβ tg slices. n = 9–16. B: Cytotoxicity in human tau expressing slices from wild-type mice treated with 1 μM recombinant Aβ. Treatment with wt Aβ42 and E22G Aβ42 but not E22Δ Aβ42, wt Aβ40, E22G Aβ40 or E22Δ Aβ40 increased cell death. n = 8–10 C: Cytotoxicity in slices from wild-type mice treated with 1 μM recombinant Aβ, in the absence of human tau expression. No toxicity was observed by wt Aβ42, E22G Aβ42 or E22Δ Aβ42 in the absence of human tau. n = 5. D: Representative western blot (left) of lysate of human tau expressing wild-type slices, treated with 1 μM recombinant Aβ, displaying total human tau, phospho-tau at the AT8 epitope and GAPDH. Quantification (right) of western blots showed increased tau phosphorylation after treatment with wt Aβ42 and E22G Aβ42 but not E22Δ Aβ42. n = 4. Data are means ± SD. Statistical significance was assessed by one-way ANOVA with Tukey's multiple comparison test (*p<0.05; **p<0.01, ***p<0.001).