Fig. 2

(Immuno-)histopathological characterization of inflammation of age-matched controls and individuals with hypertension within white matter. Representative images of ionized calcium-binding adaptor molecule 1 (IBA1) at X10 magnification of normotensive individuals (a, b) and individuals with hypertension (c, d). a, c correspond to normal-appearing white matter (NAWM) and b, d to white matter hyperintensity (WMH). The black boxes indicate regions of interest placed on the upper left corner of a–d at X20 magnification. Examination of amount of IBA1 showed more microglial activation (p = 0.01), slightly lower microglial area (p = 0.036), and a rounder/more ameboid cellular shape (p = 0.002) in individuals with hypertension (c, d) compared to controls (a, b). In WMH (b, d), we observed more microglial activation (p < 0.001), together with morphological changes in microglial cells. These changes were characterized by shortening of cellular ramifications (p = 0.014) and a rounder/more ameboid cellular shape (p < 0.001). Representative images of glial fibrillary acidic protein (GFAP) at ×10 magnification of normotensive (control) individuals (e, f) and individuals with hypertension (g, h). e, g Correspond to NAWM and f, h to WMH. Analysis of GFAP staining revealed that hypertension (g, h) leads to larger gliosis area (p = 0.005) compared to controls (e, f). Additionally, those individuals with hypertension showed an overall larger astrocytic activation (p < 0.001) than the control group. When comparing across white matter regions, WMH (f, h) showed larger GFAP positive area (p = 0.004) and astrocytic activation (p = 0.012) than NAWM (e,g). (black scale bar = 200 µm; red scale bar = 25 µm)