Cited by 149

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Blood–brain barrier dysfunction following traumatic brain injury

Alluri, Himakarnika, Wiggins-Dohlvik, Katie, Davis, Matthew L., Huang, Jason H., Tharakan, Binu·2015·Metabolic Brain Disease

Abstract

Traumatic brain injury is a serious cause of morbidity and mortality worldwide. After traumatic brain injury, the blood-brain barrier, the protective barrier between the brain and the intravascular compartment, becomes dysfunctional, leading to leakage of proteins, fluid, and transmigration of immune cells. As this leakage has profound clinical implications, including edema formation, elevated intracranial pressure and decreased perfusion pressure, much interest has been paid to better understanding the mechanisms responsible for these events. Various molecular pathways and numerous mediators have been found to be involved in the intricate process of regulating blood-brain barrier permeability following traumatic brain injury. This review provides an update to the existing knowledge about the various pathophysiological pathways and advancements in the field of blood-brain barrier dysfunction and hyperpermeability following traumatic brain injury, including the role of various tight junction proteins involved in blood-brain barrier integrity and regulation. We also address pitfalls of existing systems and propose strategies to improve the various debilitating functional deficits caused by this progressive epidemic.

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Crossref · 10.1007/s11011-015-9651-7

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  • In some situations, such as traumatic brain injury, where BBB dysfunction and plasma extravasation into the brain occurs, some astrocytes acquire a proliferative reactive phenotype.

    “In some situations, such as traumatic brain injury, where BBB dysfunction and plasma extravasation into the brain occurs, some astrocytes acquire a proliferative reactive phenotype (Alluri et al. 2015; Liddelow and Barres 2017).”

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Metadata

Authors
Alluri, H., Wiggins-Dohlvik, K., Davis, M. L., Huang, J. H., & Tharakan, B.
Venue
Metabolic Brain Disease
Published
2015-01-28
Volume
30
Issue
5
Pages
1093-1104
ISSN
  • 0885-7490
  • 1573-7365
Cited by
149
References
14
Language
en

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