Juvenile traumatic brain injury induces long-term perivascular matrix changes alongside amyloid-beta accumulation

Amandine Jullienne, Jill M. Roberts, Viorela Pop, M. Paul Murphy, Elizabeth Head, Gregory J. Bix, Jérôme Badaut

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


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.

Original languageEnglish
Pages (from-to)1637-1645
Number of pages9
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number10
StatePublished - Oct 1 2014


  • P-glycoprotein
  • amyloid
  • fibronectin
  • juvenile
  • perlecan domain V
  • traumatic brain injury

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine


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