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Neuroprotection in acute ischemic stroke – current status

With the growing understanding of the mechanism of cell death in ischemia, new approaches for treatment such as neuroprotection have emerged. The basic aim of this strategy is to interfere with the events of the ischemic cascade, blocking the pathological processes and preventing the death of nerve...

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Detalles Bibliográficos
Autores principales: Auriel, E, Bornstein, NM
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822558/
https://www.ncbi.nlm.nih.gov/pubmed/20716132
http://dx.doi.org/10.1111/j.1582-4934.2010.01135.x
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author Auriel, E
Bornstein, NM
author_facet Auriel, E
Bornstein, NM
author_sort Auriel, E
collection PubMed
description With the growing understanding of the mechanism of cell death in ischemia, new approaches for treatment such as neuroprotection have emerged. The basic aim of this strategy is to interfere with the events of the ischemic cascade, blocking the pathological processes and preventing the death of nerve cells in the ischemic penumebra. This concept involves inhibition of the pathological molecular events which eventually leads to the influx of calcium, activation of free radicals and neuronal death. Despite encouraging data from experimental animal models, all clinical trials of neuroprotective therapies have to date been unsuccessful. This article reviews some of the reasons for the failure of neuroprotection in the clinical trials so far. Despite all the negative reports, we believe it would be wrong to give up at this point, since there is still reasonable hope of finding an effective neuroprotection for stroke.
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spelling pubmed-38225582015-04-20 Neuroprotection in acute ischemic stroke – current status Auriel, E Bornstein, NM J Cell Mol Med Reviews With the growing understanding of the mechanism of cell death in ischemia, new approaches for treatment such as neuroprotection have emerged. The basic aim of this strategy is to interfere with the events of the ischemic cascade, blocking the pathological processes and preventing the death of nerve cells in the ischemic penumebra. This concept involves inhibition of the pathological molecular events which eventually leads to the influx of calcium, activation of free radicals and neuronal death. Despite encouraging data from experimental animal models, all clinical trials of neuroprotective therapies have to date been unsuccessful. This article reviews some of the reasons for the failure of neuroprotection in the clinical trials so far. Despite all the negative reports, we believe it would be wrong to give up at this point, since there is still reasonable hope of finding an effective neuroprotection for stroke. Blackwell Publishing Ltd 2010-09 2010-10-11 /pmc/articles/PMC3822558/ /pubmed/20716132 http://dx.doi.org/10.1111/j.1582-4934.2010.01135.x Text en © 2010 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
spellingShingle Reviews
Auriel, E
Bornstein, NM
Neuroprotection in acute ischemic stroke – current status
title Neuroprotection in acute ischemic stroke – current status
title_full Neuroprotection in acute ischemic stroke – current status
title_fullStr Neuroprotection in acute ischemic stroke – current status
title_full_unstemmed Neuroprotection in acute ischemic stroke – current status
title_short Neuroprotection in acute ischemic stroke – current status
title_sort neuroprotection in acute ischemic stroke – current status
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822558/
https://www.ncbi.nlm.nih.gov/pubmed/20716132
http://dx.doi.org/10.1111/j.1582-4934.2010.01135.x
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