Citation

Jullienne A, Roberts JM, Pop V, Paul Murphy M, Head E, Bix GJ, Badaut J. J. Cereb. Blood Flow Metab. 2014; 34(10): 1637-1645.

Affiliation

1] Department of Pediatrics, Loma Linda University, Loma Linda, California, USA [2] Department of Physiology, Loma Linda University, Loma Linda, California, USA [3] CNRS UMR 5287, Bordeaux University, Bordeaux, France.

Copyright

(Copyright © 2014, Nature Publishing Group)

DOI

10.1038/jcbfm.2014.124

PMID

25052558

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.

Language: en