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Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review

Aneurysmal subarachnoid hemorrhage (SAH) can lead to devastating outcomes including vasospasm, cognitive decline, and even death. Currently, treatment options are limited for this potentially life threatening injury. Recent evidence suggests that neuroinflammation plays a critical role in injury exp...

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Autores principales: Lucke-Wold, Brandon P., Logsdon, Aric F., Manoranjan, Branavan, Turner, Ryan C., McConnell, Evan, Vates, George Edward, Huber, Jason D., Rosen, Charles L., Simard, J. Marc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848953/
https://www.ncbi.nlm.nih.gov/pubmed/27049383
http://dx.doi.org/10.3390/ijms17040497
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author Lucke-Wold, Brandon P.
Logsdon, Aric F.
Manoranjan, Branavan
Turner, Ryan C.
McConnell, Evan
Vates, George Edward
Huber, Jason D.
Rosen, Charles L.
Simard, J. Marc
author_facet Lucke-Wold, Brandon P.
Logsdon, Aric F.
Manoranjan, Branavan
Turner, Ryan C.
McConnell, Evan
Vates, George Edward
Huber, Jason D.
Rosen, Charles L.
Simard, J. Marc
author_sort Lucke-Wold, Brandon P.
collection PubMed
description Aneurysmal subarachnoid hemorrhage (SAH) can lead to devastating outcomes including vasospasm, cognitive decline, and even death. Currently, treatment options are limited for this potentially life threatening injury. Recent evidence suggests that neuroinflammation plays a critical role in injury expansion and brain damage. Red blood cell breakdown products can lead to the release of inflammatory cytokines that trigger vasospasm and tissue injury. Preclinical models have been used successfully to improve understanding about neuroinflammation following aneurysmal rupture. The focus of this review is to provide an overview of how neuroinflammation relates to secondary outcomes such as vasospasm after aneurysmal rupture and to critically discuss pharmaceutical agents that warrant further investigation for the treatment of subarachnoid hemorrhage. We provide a concise overview of the neuroinflammatory pathways that are upregulated following aneurysmal rupture and how these pathways correlate to long-term outcomes. Treatment of aneurysm rupture is limited and few pharmaceutical drugs are available. Through improved understanding of biochemical mechanisms of injury, novel treatment solutions are being developed that target neuroinflammation. In the final sections of this review, we highlight a few of these novel treatment approaches and emphasize why targeting neuroinflammation following aneurysmal subarachnoid hemorrhage may improve patient care. We encourage ongoing research into the pathophysiology of aneurysmal subarachnoid hemorrhage, especially in regards to neuroinflammatory cascades and the translation to randomized clinical trials.
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spelling pubmed-48489532016-05-04 Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review Lucke-Wold, Brandon P. Logsdon, Aric F. Manoranjan, Branavan Turner, Ryan C. McConnell, Evan Vates, George Edward Huber, Jason D. Rosen, Charles L. Simard, J. Marc Int J Mol Sci Review Aneurysmal subarachnoid hemorrhage (SAH) can lead to devastating outcomes including vasospasm, cognitive decline, and even death. Currently, treatment options are limited for this potentially life threatening injury. Recent evidence suggests that neuroinflammation plays a critical role in injury expansion and brain damage. Red blood cell breakdown products can lead to the release of inflammatory cytokines that trigger vasospasm and tissue injury. Preclinical models have been used successfully to improve understanding about neuroinflammation following aneurysmal rupture. The focus of this review is to provide an overview of how neuroinflammation relates to secondary outcomes such as vasospasm after aneurysmal rupture and to critically discuss pharmaceutical agents that warrant further investigation for the treatment of subarachnoid hemorrhage. We provide a concise overview of the neuroinflammatory pathways that are upregulated following aneurysmal rupture and how these pathways correlate to long-term outcomes. Treatment of aneurysm rupture is limited and few pharmaceutical drugs are available. Through improved understanding of biochemical mechanisms of injury, novel treatment solutions are being developed that target neuroinflammation. In the final sections of this review, we highlight a few of these novel treatment approaches and emphasize why targeting neuroinflammation following aneurysmal subarachnoid hemorrhage may improve patient care. We encourage ongoing research into the pathophysiology of aneurysmal subarachnoid hemorrhage, especially in regards to neuroinflammatory cascades and the translation to randomized clinical trials. MDPI 2016-04-02 /pmc/articles/PMC4848953/ /pubmed/27049383 http://dx.doi.org/10.3390/ijms17040497 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Lucke-Wold, Brandon P.
Logsdon, Aric F.
Manoranjan, Branavan
Turner, Ryan C.
McConnell, Evan
Vates, George Edward
Huber, Jason D.
Rosen, Charles L.
Simard, J. Marc
Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review
title Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review
title_full Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review
title_fullStr Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review
title_full_unstemmed Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review
title_short Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review
title_sort aneurysmal subarachnoid hemorrhage and neuroinflammation: a comprehensive review
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848953/
https://www.ncbi.nlm.nih.gov/pubmed/27049383
http://dx.doi.org/10.3390/ijms17040497
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