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Fig. 8 | Translational Neurodegeneration

Fig. 8

From: Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer’s disease protects against mitochondrial dysfunction and mitigates brain pathology

Fig. 8

VBIT-4 treatment of 5 × FAD mice improves astrocyte and microglia morphology and activates microglia. a Confocal images of cortical sections from WT, untreated-, and VBIT-4-treated-5 × FAD mice co-immunostained for VDAC1 and GFAP. b Quantification of GFAP intensity in cortical and hippocampal sections. ce Spinning disk microscopy 3D imaging of 50 μm cortical sections from 5 × FAD, and VBIT-4-treated-5 × FAD mice co-immunostained for GFAP and VDAC1 (c), analyzed using Imaris software for astrocyte 3D structures (c), number of branching points as a function of the distance from the soma (d) and number of processes for each branch order (e). f Cortical sections from WT, VBIT-4-treated, and untreated 5 × FAD mice were co-immunostained for VDAC1 and IBA-1. Higher magnifications of selected areas are shown. g Quantitative analysis of IBA-1 expression levels in and outside the Aβ plaques. hl Spinning disk microscopy 3D imaging of 50 μm cortical sections from VBIT-4-treated- and untreated-5 × FAD mice stained for IBA-1 shown in 3D, as analyzed using Imaris software (h). Representative microglia structures in the Aβ plaques are shown at the bottom, and number of processes for each branch order (i) and the number of branching points as a function of the distance from soma (j). k, l Confocal images of cortical sections from WT, VBIT-4-treated, and untreated-5 × FAD mice co-immunostained for TSPO and VDAC1 (k) and quantification of staining intensity in the Aβ plaques (l). Results show means ± SEM (n = 3), ***P < 0.001, ****P < 0.0001. P-value in blue color represents the significance of VBIT-4-treated relative to untreated 5 × FAD mice. NS, not significant

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