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Figure 4 | Molecular Neurodegeneration

Figure 4

From: Tau deletion impairs intracellular β-amyloid-42 clearance and leads to more extracellular plaque deposition in gene transfer models

Figure 4

Aβ1-42 is more efficiently cleared in WT than Tau−/−mice. Staining of 20 μm thick coronal sections with p-Tau (AT8) and counterstained with DAB in A) LacZ + DMSO, B) Tau + DMSO, C) Tau + Nilotinib, D) Tau and Aβ1-42 + DMSO and E) Tau and Aβ1-42 + Nilotinib. Staining of hippocampus with AT8 and DAB in F) LacZ + DMSO, G) Tau + DMSO, H) Tau + Nilotinib, I) Tau and Aβ1-42 + DMSO and J) Tau and Aβ1-42 + Nilotinib in Tau−/− mice. Staining of 20 μm thick coronal sections with p-Tau (AT180) and DAB in K) LacZ + DMSO, L) Tau + DMSO, M) Tau + Nilotinib, N) Tau and Aβ1-42 + DMSO and O) Tau and Aβ1-42 + Nilotinib in WT mice. Staining of cortical sections in P) LacZ + DMSO, Q) Tau + DMSO, R) Tau + Nilotinib, S) Tau and Aβ1-42 + DMSO and T) Tau and Aβ1-42 + Nilotinib in Tau−/− mice. U) Histograms represent stereological quantification of p-Tau. Asterisk indicates significantly different to Aβ1-42 + DMSO, bars are mean ± SEM, two-way ANOVA.

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