The rise and fall of NMDA antagonists for ischemic stroke.

It has long been accepted that high concentrations of glutamate can destroy neurons, and this is the basis of the theory of excitotoxicity during brain injury such as stroke. Glutamate N-methyl-D-aspartate (NMDA) receptor antagonists such as Selfotel, Aptiganel, Gavestinel and others failed to show...

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Main Authors: Hoyte, L, Barber, P, Buchan, A, Hill, MD
Format: Journal article
Language:English
Published: 2004
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author Hoyte, L
Barber, P
Buchan, A
Hill, MD
author_facet Hoyte, L
Barber, P
Buchan, A
Hill, MD
author_sort Hoyte, L
collection OXFORD
description It has long been accepted that high concentrations of glutamate can destroy neurons, and this is the basis of the theory of excitotoxicity during brain injury such as stroke. Glutamate N-methyl-D-aspartate (NMDA) receptor antagonists such as Selfotel, Aptiganel, Gavestinel and others failed to show neuroprotective efficacy in human clinical trials or produced intolerable central nervous system adverse effects. The failure of these agents has been attributed to poor studies in animal models and to poorly designed clinical trials. We also speculate that NMDA receptor antagonism may have hindered endogenous mechanisms for neuronal survival and neuroregeneration. It remains to be proven in human stroke whether NMDA receptor antagonism can be neuroprotective.
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spelling oxford-uuid:ec69143d-e610-49d4-b5a8-c25a15c15aa52022-03-27T11:17:15ZThe rise and fall of NMDA antagonists for ischemic stroke.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:ec69143d-e610-49d4-b5a8-c25a15c15aa5EnglishSymplectic Elements at Oxford2004Hoyte, LBarber, PBuchan, AHill, MDIt has long been accepted that high concentrations of glutamate can destroy neurons, and this is the basis of the theory of excitotoxicity during brain injury such as stroke. Glutamate N-methyl-D-aspartate (NMDA) receptor antagonists such as Selfotel, Aptiganel, Gavestinel and others failed to show neuroprotective efficacy in human clinical trials or produced intolerable central nervous system adverse effects. The failure of these agents has been attributed to poor studies in animal models and to poorly designed clinical trials. We also speculate that NMDA receptor antagonism may have hindered endogenous mechanisms for neuronal survival and neuroregeneration. It remains to be proven in human stroke whether NMDA receptor antagonism can be neuroprotective.
spellingShingle Hoyte, L
Barber, P
Buchan, A
Hill, MD
The rise and fall of NMDA antagonists for ischemic stroke.
title The rise and fall of NMDA antagonists for ischemic stroke.
title_full The rise and fall of NMDA antagonists for ischemic stroke.
title_fullStr The rise and fall of NMDA antagonists for ischemic stroke.
title_full_unstemmed The rise and fall of NMDA antagonists for ischemic stroke.
title_short The rise and fall of NMDA antagonists for ischemic stroke.
title_sort rise and fall of nmda antagonists for ischemic stroke
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