Fig. 4
From: APOEε4 alters ApoE and Fabp7 in frontal cortex white matter in prodromal Alzheimer's disease

FC WM Olig2 positive cells in NCI, MCI, and AD APOEε4 carriers and non-carriers. A–L Low magnification images of Olig2 (purple) reactivity in the WM (dashed lines) in APOEε3 (A–C) and APOEε4 (G–I) carriers. Higher power images of WM Olig2 immunoreactive cells in APOEε3 (D–F) and APOEε4 (J–L) WM displaying a small oval-shaped morphology in all clinical and genotype groups. Boxed insects show high power images of Olig2 positive cells in each panel (e.g., arrows in L). Scale bar in I = 250 μm and applies to panels A–C, G–I. Scale bar in L = 25 μm and inset = 10 μm applies to panels (D–F, J–L). M Quantification revealed a significant decrease in Olig2-positive nuclei in AD compared to NCI in APOEε4 non-carriers and in MCI carriers compared to non-carriers (NCI3/3 n = 11, MCI3/3 n = 10, AD3/3 n = 9, NCI3/4 n = 9, MCI3/4 n = 9, AD3/4 n = 9). Data shown in bar graph is presented as mean ± SEM. Statistical significance was determined using the Kruskal–Wallis followed by a Dunn’s test for comparisons across clinical groups and Mann–Whitney test for comparisons between carriers and non-carriers within each clinical group. Significance levels (*) were set at: *p < 0.05, **p < 0.01, ***p < 0.001. GM grey matter, WM white matter