@article{ref1,
title="Juvenile traumatic brain injury induces long-term perivascular matrix changes alongside amyloid-beta accumulation",
journal="Journal of cerebral blood flow and metabolism",
year="2014",
author="Jullienne, Amandine and Roberts, Jill M. and Pop, Viorela and Paul Murphy, M. and Head, Elizabeth and Bix, Gregory J. and Badaut, Jerome",
volume="34",
number="10",
pages="1637-1645",
abstract="In our juvenile traumatic brain injury (jTBI) model, emergence of cognitive dysfunctions was observed up to 6 months after trauma. Here we hypothesize that early brain injury induces changes in the neurovascular unit (NVU) that would be associated with amyloid-beta (Aβ) accumulation. We investigated NVU changes for up to 6 months in a rat jTBI model, with a focus on the efflux protein P-glycoprotein (P-gp) and on the basement membrane proteins perlecan and fibronectin, all known to be involved in Aβ clearance. Rodent-Aβ staining is present and increased after jTBI around cerebral blood microvessels, and the diameter of those is decreased by 25% and 34% at 2 and 6 months, respectively, without significant angiogenesis. P-glycoprotein staining in endothelium is decreased by 22% and parallels an increase of perlecan and fibronectin staining around cerebral blood vessels. Altogether, these results strongly suggest that the emergence of long-term behavioral dysfunctions observed in rodent jTBI may be related to endothelial remodeling at the blood-brain barrier alongside vascular dysfunction and altered Aβ trafficking. This study shows that it is important to consider jTBI as a vascular disorder with long-term consequences on cognitive functions.Journal of Cerebral Blood Flow & Metabolism advance online publication, 23 July 2014; doi:10.1038/jcbfm.2014.124.<p /> <p>Language: en</p>",
language="en",
issn="0271-678X",
doi="10.1038/jcbfm.2014.124",
url="http://dx.doi.org/10.1038/jcbfm.2014.124"
}