Fig. 2

Aged mice display exacerbated S100β⁺Vim⁺ reactive astrogliosis in the hippocampus but not the neocortex following TBI. Serial sections comprising the dorsal hippocampus were imaged for S100β (i) and Vimentin (ii) as a colocalization image (iii). Pixel positive area was defined for each stain using young sham’s levels. HALO colocalization algorithm was used to compute the total colocalized area for both S100β (green, iv) and Vimentin (red, iv), which was represented as the dual-positive staining fraction (yellow, iv). Dual-positive astrocytes were increasingly reactive as a function of time after injury for aged mice, which show a progressive accumulation peaking at 7 days post-injury. Comparatively, young mice display relatively little change as a result of TBI at any time post-injury. ANOVA revealed significant differences in the hippocampus due to age (F (1, 28) = 33.61, P < 0.0001), interval (F (3, 28) = 10.38, P < 0.0001), and their interaction (F (3, 28) = 5.831, P = 0.0032). However, no significant effects for age, interval, or their interaction were observed for these measures in the neocortex. **P < 0.01 for pairwise comparisons of 3-day and 7-day intervals between young and aged mice. n = 4–5/group. Data are presented as mean ± SEM. Young, gray bars; Aged, blue bars. Scale bar is 50 μm