Blood-brain barrier disruption is an early event that may persist for many years after traumatic brain injury in humans

Hay, J. R., Johnson, V. E., Young, A. M.H., Smith, D. H. and Stewart, W. (2015) Blood-brain barrier disruption is an early event that may persist for many years after traumatic brain injury in humans. Journal of Neuropathology and Experimental Neurology, 74(12), pp. 1147-1157. (doi: 10.1097/NEN.0000000000000261) (PMID:26574669)

Abstract

Traumatic brain injury (TBI) is a risk factor for dementia. Mixed neurodegenerative pathologies have been described in late survivors of TBI, but the mechanisms driving post-TBI neurodegeneration remain elusive. Increasingly, blood-brain barrier (BBB) disruption has been recognized in a range of neurologic disorders including dementias, but little is known of the consequences of TBI on the BBB. Autopsy cases of single moderate or severe TBI from the Glasgow TBI Archive (n = 70) were selected to include a range from acute (10 hours–13 days) to long-term (1–47 years) survival, together with age-matched uninjured controls (n = 21). Multiple brain regions were examined using immunohistochemistry for the BBB integrity markers fibrinogen and immunoglobulin G. After TBI, 40% of patients dying in the acute phase and 47% of those surviving a year or more from injury showed multifocal, abnormal, perivascular, and parenchymal fibrinogen and immunoglobulin G immunostaining localized to the gray matter, with preferential distribution toward the crests of gyri and deep neocortical layers. In contrast, when present, controls showed only limited localized immunostaining. These preliminary data demonstrate evidence of widespread BBB disruption in a proportion of TBI patients emerging in the acute phase and, intriguingly, persisting in a high proportion of late survivors.

• Item Type: Articles
• Additional Information: This study was supported by National Institutes of Health Grants NS038104 and NS056202; US Department of Defense Grant PT110785; and The Sackler Institute Endowment Fund, Department of Neurology, Queen Elizabeth University Hospital, Glasgow, United Kingdom.
• Status: Published
• Refereed: Yes
• Glasgow Author(s) Enlighten ID: Stewart, Dr William and Hay, Dr Jennifer
• Authors: Hay, J. R., Johnson, V. E., Young, A. M.H., Smith, D. H., and Stewart, W.
• College/School: College of Medical Veterinary and Life Sciences > School of Psychology & Neuroscience; College of Medical Veterinary and Life Sciences > School of Medicine, Dentistry & Nursing
• Journal Name: Journal of Neuropathology and Experimental Neurology
• Publisher: Lippincott, Williams & Wilkins
• ISSN: 0022-3069
• ISSN (Online): 1554-6578
• Published Online: 01 December 2015
• Copyright Holders: Copyright © 2015 American Association of Neuropathologists, Inc.
• First Published: First published in Journal of Neuropathology and Experimental Neurology 74(12):1147-1157
• Publisher Policy: Reproduced in accordance with the copyright policy of the publisher