Fig. 4

Effect of VBIT-4 treatment on the levels of Aβ plaques, and the expression of p-Tau and PrPc in the 5 × FAD brain. a Brain sections from 5 × FAD mice were immunostained for Aβ using anti-Aβ antibodies. The cerebral cortex and hippocampal formation that were analyzed in this study are enlarged in (i) and (ii) panels. The CA1 (cornu ammonis subfield 1), ML (molecular layers), GCL (granule cell layer), and DG (dentate gyrus) are indicated. b Representative thioflavin-S (Thio-s) staining of Aβ plaques in cortical and hippocampal sections from VBIT-4-treated and untreated 5 × FAD mice. c, d Areas occupied by Aβ plaques in the cortex (c) and hippocampus (d), as analyzed from Thio-s or anti-Aβ antibodies (anti-Aβ), are expressed as mean ± SE (n = 5–9 as indicated). e–h IF staining and quantification of p-Tau and VDAC1 (e, f), and of VDAC1 and PrPc (g, h) in cortical sections from WT and VBIT-4-treated and untreated 5 × FAD mice. and their quantification. Results show means ± SEM (n = 3 animals for each group, with  IF was performed 2–3 times for each group), **P < 0.01, ***P < 0.001, ****P < 0.0001. NS, not significant. p-value in blue color represents the significance of VBIT-4-treated 5 × FAD mice relative to untreated mice