Controlled cortical impact (CCI) causes intra-axonal Aβ accumulation in young 3xTg-AD mice at 24 hours.

<p><b>A</b>. Immunoprecipitation (IP) and Western blot (WB) showed that HJ3.4 antibody, similar to 82E1 antibody, did not recognize APP, while, 6E10 antibody recognized APP. <b>B</b>. Representative Cresyl violet stained sections showing white matter regions (boxes) with positive axonal Aβ pathology following TBI in 3xTg-AD mice (Modified from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0025475#pone.0025475-Franklin1" target="_blank">[46]</a>). <b>C–J</b>. HJ3.4 staining in uninjured (sham) and injured (CCI) 3xTg-AD mice, counterstained with Cresyl violet. Intra-axonal Aβ accumulation was observed in the ipsilateral fimbria (<b>C–D</b>, black box in <b>B</b>), ipsilateral hippocampal commissure (<b>E–F</b>, blue box in <b>B</b>), ipsilateral corpus callosum (<b>G–H</b>, red box in <b>B</b>) and ipsilateral external capsule (<b>I–J</b>, purple box in <b>B</b>) of injured 3xTg-AD mice. Scale bar in <b>C</b>: 50 µm. Most prominent Aβ staining was observed in the ipsilateral fimbria/fornix of injured mice. Aβ staining has beads-on-a-string and varicose morphologies, consistent with morphologies of injured axons.