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Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions
The translation of neuroprotective agents for ischemic stroke from bench-to-bedside has largely failed to produce improved treatments since the development of tissue plasminogen activator (tPA). One possible reason for lack of translation is the failure to acknowledge the greatest risk factor for st...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565354/ https://www.ncbi.nlm.nih.gov/pubmed/23344061 http://dx.doi.org/10.3390/ijms14011890 |
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author | Turner, Ryan C. Lucke-Wold, Brandon Lucke-Wold, Noelle Elliott, Alisa S. Logsdon, Aric F. Rosen, Charles L. Huber, Jason D. |
author_facet | Turner, Ryan C. Lucke-Wold, Brandon Lucke-Wold, Noelle Elliott, Alisa S. Logsdon, Aric F. Rosen, Charles L. Huber, Jason D. |
author_sort | Turner, Ryan C. |
collection | PubMed |
description | The translation of neuroprotective agents for ischemic stroke from bench-to-bedside has largely failed to produce improved treatments since the development of tissue plasminogen activator (tPA). One possible reason for lack of translation is the failure to acknowledge the greatest risk factor for stroke, age, and other common comorbidities such as hypertension, obesity, and diabetes that are associated with stroke. In this review, we highlight both mechanisms of studying these factors and results of those that have been addressed. We also discuss the potential role of other lifestyle factors associated with an increased stroke risk such as sleep fragmentation and/or deprivation. Furthermore, many proposed therapeutic agents have targeted molecular mechanisms occurring soon after the onset of ischemia despite data indicating delayed patient presentation following ischemic stroke. Modulating inflammation has been identified as a promising therapeutic avenue consistent with preliminary success of ongoing clinical trials for anti-inflammatory compounds such as minocycline. We review the role of inflammation in stroke and in particular, the role of inflammatory cell recruitment and macrophage phenotype in the inflammatory process. Emerging evidence indicates an increasing role of neuro-immune crosstalk, which has led to increased interest in identification of peripheral biomarkers indicative of neural injury. It is our hope that identification and investigation of factors influencing stroke pathophysiology may lead to improved therapeutics. |
format | Online Article Text |
id | pubmed-3565354 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-35653542013-03-13 Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions Turner, Ryan C. Lucke-Wold, Brandon Lucke-Wold, Noelle Elliott, Alisa S. Logsdon, Aric F. Rosen, Charles L. Huber, Jason D. Int J Mol Sci Review The translation of neuroprotective agents for ischemic stroke from bench-to-bedside has largely failed to produce improved treatments since the development of tissue plasminogen activator (tPA). One possible reason for lack of translation is the failure to acknowledge the greatest risk factor for stroke, age, and other common comorbidities such as hypertension, obesity, and diabetes that are associated with stroke. In this review, we highlight both mechanisms of studying these factors and results of those that have been addressed. We also discuss the potential role of other lifestyle factors associated with an increased stroke risk such as sleep fragmentation and/or deprivation. Furthermore, many proposed therapeutic agents have targeted molecular mechanisms occurring soon after the onset of ischemia despite data indicating delayed patient presentation following ischemic stroke. Modulating inflammation has been identified as a promising therapeutic avenue consistent with preliminary success of ongoing clinical trials for anti-inflammatory compounds such as minocycline. We review the role of inflammation in stroke and in particular, the role of inflammatory cell recruitment and macrophage phenotype in the inflammatory process. Emerging evidence indicates an increasing role of neuro-immune crosstalk, which has led to increased interest in identification of peripheral biomarkers indicative of neural injury. It is our hope that identification and investigation of factors influencing stroke pathophysiology may lead to improved therapeutics. MDPI 2013-01-17 /pmc/articles/PMC3565354/ /pubmed/23344061 http://dx.doi.org/10.3390/ijms14011890 Text en © 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Review Turner, Ryan C. Lucke-Wold, Brandon Lucke-Wold, Noelle Elliott, Alisa S. Logsdon, Aric F. Rosen, Charles L. Huber, Jason D. Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions |
title | Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions |
title_full | Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions |
title_fullStr | Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions |
title_full_unstemmed | Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions |
title_short | Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions |
title_sort | neuroprotection for ischemic stroke: moving past shortcomings and identifying promising directions |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565354/ https://www.ncbi.nlm.nih.gov/pubmed/23344061 http://dx.doi.org/10.3390/ijms14011890 |
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