Fig. 2: Intra-subject variability of Musashi deposition in AD, ALS, and FTD frontal cortex.
From: RNA-binding proteins Musashi and tau soluble aggregates initiate nuclear dysfunction
a Schematic approach to study MSI1, MSI2 and Tau deposition in human diseased brains. b Representative confocal image of nuclei stained with MSI1, TOMA-2 and DAPI in control (Ctr) brains. c Confocal images of cortical AD brain showed nuclei stained with MSI1, TOMA-2, and DAPI, three different nuclei are represented for each field the pixel distribution graph and colocalization pixel map has been reported. d Confocal images of cortical FTD brain showed nuclei stained with MSI1, TOMA-2 and DAPI, three different nuclei are represented for each field the pixel distribution graph and colocalization pixel map has been reported. e Confocal images of cortical ALS brain showed nuclei stained with MSI1, TOMA-2 and DAPI, three different nuclei are represented for each field the pixel distribution graph and colocalization pixel map has been reported. In all images merge is presented with MSI1 (green), TOMA-2 (red) and DAPI (blue) white scale bar: 2 µm. f PCC comparison between MSI1 and TOMA-2 intensities, significant co-localization has been observed between control and diseased brains. In particular, Ctr vs. AD ***, Ctr vs. ALS *, Ctr vs FTD **, Dunnett’s multiple comparisons test One-way ANOVA has been performed with a p-value=0.0006 between columns. N = 3 biologically independent cells (ROIs) examined over three independent experiments. Data are presented as mean ± SD. g MSI1 and MSI2 soluble and insoluble fraction from Ctr, AD, ALS, and FTD human brains, presented in duplicate. h Tau soluble and insoluble fractions from Ctr, AD, ALS, FTD human brains, presented in duplicate.
