TY  - JOUR
PY  - 2014//
TI  - Juvenile traumatic brain injury induces long-term perivascular matrix changes alongside amyloid-beta accumulation
JO  - Journal of cerebral blood flow and metabolism
A1  - Jullienne, Amandine
A1  - Roberts, Jill M.
A1  - Pop, Viorela
A1  - Paul Murphy, M.
A1  - Head, Elizabeth
A1  - Bix, Gregory J.
A1  - Badaut, Jerome
SP  - 1637
EP  - 1645
VL  - 34
IS  - 10
N2  - 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>
LA  - en
SN  - 0271-678X
UR  - http://dx.doi.org/10.1038/jcbfm.2014.124
ID  - ref1
ER  -