Fig. 3

Amyloid precursor protein (APP) is upregulated following rmTBI. a–j Representative immunohistochemical photomicrographs demonstrate APP expression (arrows) in the corpus callosum and prefrontal cortex, in control sections (a, b) and at 48 h (c, d), 1 w (e, f), 4 w (g, h) and 10 w (i, j) post-rmTBI, respectively. Scale bar = 50 μm. (k, l) Western blot and densitometric analyses of full-length APP in the cortex of sham mice, 48 h after the last sham procedure, and in rmTBI mice at 8 h, 48 h, 1 w and 20 w post-rmTBI, demonstrate a significant increase in APP levels at 8 h, 48 h and 1 w, post injury that resolves to baseline levels at 20 w post injury. β-actin levels were used as a protein loading control. Asterisk indicates statistically different from shams, p < 0.05; one-way ANOVA