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Re-exploring Tumor Necrosis Factor Alpha as a Target for Therapy in Intracerebral Hemorrhage

Re-exploring Tumor Necrosis Factor Alpha as a Target for Therapy in Intracerebral Hemorrhage Intracerebral hemorrhage (ICH) is a perplexing condition with high mortality and no treatment beyond supportive care. A major portion of the injurious process is takes place during the hours following the development of hematoma. This so-called secondary injury is characterized by an inflammatory cascade that involves a variety of cytokines, including tumor necrosis factor (TNF)-α. Several studies in the rodent model of ICH have shown a rapid increase in brain concentrations of TNF-α following hematoma induction. There is a reasonable body of evidence from experimental models of ICH suggesting that upregulation of TNF-α adjacent to the hematoma is associated with increased peri-hematomal edema, and that inhibition of TNF-α attenuates the formation and progression of this edema and ultimately improves outcomes. Unfortunately, efforts to expand upon these findings have interminably stalled at the pre-clinical phase. A robust clinical study to validate serum TNF-α as a marker for secondary injury in ICH patients is yet to materialize. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Translational Stroke Research Springer Journals

Re-exploring Tumor Necrosis Factor Alpha as a Target for Therapy in Intracerebral Hemorrhage

Behrouz, Réza
Translational Stroke Research , Volume 7 (2) – Jan 14, 2016
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References (31)

Publisher
Springer Journals
Copyright
Copyright © 2016 by Springer Science+Business Media New York
Subject
Biomedicine; Neurosciences; Neurology; Cardiology; Neurosurgery; Vascular Surgery
ISSN
1868-4483
eISSN
1868-601X
DOI
10.1007/s12975-016-0446-x
pmid
26762364
Publisher site
See Article on Publisher Site

Abstract

Intracerebral hemorrhage (ICH) is a perplexing condition with high mortality and no treatment beyond supportive care. A major portion of the injurious process is takes place during the hours following the development of hematoma. This so-called secondary injury is characterized by an inflammatory cascade that involves a variety of cytokines, including tumor necrosis factor (TNF)-α. Several studies in the rodent model of ICH have shown a rapid increase in brain concentrations of TNF-α following hematoma induction. There is a reasonable body of evidence from experimental models of ICH suggesting that upregulation of TNF-α adjacent to the hematoma is associated with increased peri-hematomal edema, and that inhibition of TNF-α attenuates the formation and progression of this edema and ultimately improves outcomes. Unfortunately, efforts to expand upon these findings have interminably stalled at the pre-clinical phase. A robust clinical study to validate serum TNF-α as a marker for secondary injury in ICH patients is yet to materialize.

Journal

Translational Stroke Research – Springer Journals

Published: Jan 14, 2016

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