Skip to main content
Fig. 8 | Molecular Neurodegeneration

Fig. 8

From: Multiscale network modeling of oligodendrocytes reveals molecular components of myelin dysregulation in Alzheimer’s disease

Fig. 8

Downregulation of AD-associated proteins in mice lacking the oligodendrocyte network key driver Cnp. a Representative western blots of BIN1, GOT2, CNP and alpha-TUBULIN stainings on Cnp-WT and Cnp-KO corpus callosum (CC) tissues (n = 3). b Quantification of BIN1 and GOT2 protein expression in Cnp-KO corpus callosum compared to Cnp-WT corpus callosum (protein expression normalized to alpha-TUBULIN expression for each sample, n = 3 per condition; p = 0.0041, p = 0.0007, p = 0.032). c Representative confocal image of post-natal day 60 sections of Cnp-WT and Cnp-KO corpus callosum, stained for OLIG2 (red), BIN1 (green) and DAPI (blue), scale bar = 300 μm. The bottom panel shows higher magnification of the double stainings (white arrowheads indicate double positive for BIN1 and OLIG2), scale bar = 50 μm. d Quantification of the proportion of each cell types expressing BIN1 in Cnp-WT and Cnp-KO corpus callosum (oligodendrocytes – OLIG2+ in gray, neurons – NeuN+ in white, astrocytes – GFAP+ in black; n = 3–4). e Quantification of the percentage of OLIG2+ cells expressing BIN1 in Cnp-WT and Cnp-KO corpus callosum (n = 3–4). f Representative confocal image of post-natal day 60 sections of Cnp-WT and Cnp-KO cortex, stained for OLIG2 or NeuN (red), GOT2 (green) and DAPI (blue), scale bar = 300 μm. The bottom panel shows magnification of the double stainings (white arrowheads indicate double positive for GOT2 and OLIG2 or NeuN, respectively), scale bar = 50 μm. g Quantification of the proportion of each cell types expressing GOT2 in Cnp-WT and Cnp-KO cortex (oligodendrocytes – OLIG2+ in gray, neurons – NeuN+ in white, astrocytes – GFAP+ in black; n = 3–4). h Quantification of the percentage of OLIG2+ cells and of NeuN+ cells expressing GOT2 in Cnp-WT and Cnp-KO corpus callosum (n = 3–4). * p < 0.05, ** p < 0.01, *** p < 0.001

Back to article page