Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 33, Issue 2, Pages 205-214Publisher
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2012.154
Keywords
amyloid; claudin 5; endothelial; juvenile; P-glycoprotein; traumatic brain injury
Categories
Funding
- NSF [MRI-DBI 0923559]
- Direct For Biological Sciences
- Div Of Biological Infrastructure [923559] Funding Source: National Science Foundation
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Clinical studies suggest that traumatic brain injury (TBI) hastens cognitive decline and development of neuropathology resembling brain aging. Blood-brain barrier (BBB) disruption following TBI may contribute to the aging process by deregulating substance exchange between the brain and blood. We evaluated the effect of juvenile TBI (jTBI) on these processes by examining long-term alterations of BBB proteins, beta-amyloid (A beta) neuropathology, and cognitive changes. A controlled cortical impact was delivered to the parietal cortex of male rats at postnatal day 17, with behavioral studies and brain tissue evaluation at 60 days post-injury (dpi). Immunoglobulin G extravasation was unchanged, and jTBI animals had higher levels of tight-junction protein claudin 5 versus shams, suggesting the absence of BBB disruption. However, decreased P-glycoprotein (P-gp) on cortical blood vessels indicates modifications of BBB properties. In parallel, we observed higher levels of endogenous rodent A beta in several brain regions of the jTBI group versus shams. In addition at 60 dpi, jTBI animals displayed systematic search strategies rather than relying on spatial memory during the water maze. Together, these alterations to the BBB phenotype after jTB1 may contribute to the accumulation of toxic products, which in turn may induce cognitive differences and ultimately accelerate brain aging. Journal of Cerebral Blood Flow & Metabolism (2013) 33, 205-214; doi:10.1038/jcbfm.2012.154; published online 14 November 2012
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