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Fig. 1 | Fluids and Barriers of the CNS

Fig. 1

From: Chronic effects of blast injury on the microvasculature in a transgenic mouse model of Alzheimer’s disease related Aβ amyloidosis

Fig. 1

Cortical Aβ load after bTBI in APP/PS1 mice at 3-months and 12-months survival. AE A whole hemisphere coronal section stained for Nissl substance (obtained from the Allen Brain Atlas) illustrates the cytoarchitecture of the cortical area targeted (A; purple cresyl violet signal) and Aβ-immunostained sections illustrating Aβ pathology load (BE) in transgenic mice undergoing Sham or bTBI exposure and evaluated at 3-months survival (B and C, respectively) or at 12-months survival (D and E, respectively). F, G Graphs showing percent area coverage of Aβ-immunoreactive deposits (F) and cyano-PiB labeled amyloid pathology (G). Wild type mice are not shown as they were free of Aβ immunolabeling and cyano-PiB fluorescence. CTX, neocortex; HPC, hippocampus; THAL, thalamus. N = 3 mice/group. One-way ANOVA: F (3, 8) = 229.9, P < 0.0001 [Aβ (6E10) immunohistochemistry]; F (3, 8) = 94.10, P < 0.0001 (cyano-PiB). Brackets indicate differences of P < 0.05

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