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Fig. 7 | Translational Neurodegeneration

Fig. 7

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

Fig. 7

VBIT-4 treatment of 5 × FAD mice protects against cell metabolic impairments. a Confocal images of cortical sections from WT, untreated- and VBIT-4-treated-5 × FAD mice co-immunostained for glucose transporters: Glut-1 and GFAP, showing localization in astrocytes’ dendritic end-feet touching the blood vessels (white arrows), magnified in (i), Glut-2 co-stained with IBA-1 and Glut-4. b Glu-1,2,4 quantifications. (c) q-RT-PCR analysis of Glut-1 mRNA levels. dg Cortical sections from the three groups co-stained for VDAC1 and HK-I, with a magnification of the selected area (ii), CS, or ATP synthase (ATPsyn5a) and their quantification in cortex and hippocampus (eg). h, i Co-staining of Na,K-ATPase and VDAC1 and their quantification. Results show means ± SEM (n = 3), *P < 0.05, **P < 0.01, ***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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