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Blood–brain barrier dysfunction following traumatic brain injury
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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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).”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Alluri et al. 2015
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“Cytotoxic edema occurs when energy pumps fail and mitochondria are damaged, leading to accumulation of water with resultant swelling in neurons, glia and astrocytes (Greve and Zink 2009; Xi et al. 2002).”
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Baumart, G. J., Rodrigues, M. S., Sholl, J. N., de Sousa, A. C., Weber, A. F., Costa‐Beber, L. C., Farias, H. R., Costa, M. V., Peres, A. M., de Camargo, P. R., et al. (2026) · Journal of Neurochemistry · doi:10.1111/jnc.70403 · Cited by 2
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
- Licence
- www.springer.com/tdm (tdm)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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