Fig. 2

Temporal and spatial distribution of p-Tau pathology in neurons and astroglia. (a,b) Double staining indicates colocalization (white arrows) of hyperphosphorylated tau (p-Tau; AT8) with (a) neurons (NeuN) and (b) astrocytes (GFAP) in the cerebral cortex at 4 weeks after repetitive traumatic brain injury (rTBI). White scale bars correspond to 50 µm in low power and 17 µm in high power magnified panels. DAPI (blue) channel omitted from high power magnifications. (c) Dotted lines delineate cortical layers I-III (superficial cortex) from cortical layers IV-VI (deep cortex) and corpus callosum used to assess the presence of p-Tau stained cells in the ipsilateral hemisphere. Asterisk denotes the approximate location of the images taken for a-b. (d) Proportion of AT8 positive neurons and astrocytes at the investigated time points after rTBI. (e) Distribution of AT8 stained cells in the cerebral cortex (superficial + deep combined) relative to the impact center (black bars). There was no difference in the number and distribution of p-Tau positive cells at 4 weeks and 24 weeks after rTBI (P > 0.05). Because sham and 1-week rTBI animals had no cortical AT8-positive cells they were omitted from this analysis. Each bar corresponds to one cortical field of view (FOV) arranged from left, contralateral (FOV 1) to right, ipsilateral (FOV 16), whereby corresponding FOVs in the three investigated sections s1–s3 were summed. Data are mean ± SD. (f) Number of p-Tau positive neurons (green shades) and astrocytes (blue shades) in the traumatized hemisphere stratified by location in the superficial cortex, deep cortex, and corpus callosum over time (total number of cells counted in the three investigated sections s1–s3). *P < 0.05. Data are mean ± SEM. n = 8 mice for sham, 1 week, and 4 weeks, n = 4 for 24 weeks (there were no p-Tau positive cells in sham operated mice). All analyses were done using one-way ANOVA on Ranks with post-hoc Dunn's