Abstract
Cardiopulmonary arrest is one of the leading causes of death and disability, primarily occurring in the aged population. Numerous global cerebral ischemia animal models induce neuronal damage similar to cardiac arrest. These global cerebral ischemia models range from vessel occlusion to total cessation of cardiac function, both of which have allowed for the investigation of this multifaceted disease and detection of numerous agents that are neuroprotective. Synapses endure a variety of alterations after global cerebral ischemia from the resulting excitotoxicity and have been a major target for neuroprotection; however, neuroprotective agents have proven unsuccessful in clinical trials, as neurological outcomes have not displayed significant improvements in patients. A majority of these neuroprotective agents have specific neuronal targets, where the success of future neuroprotective agents may depend on non-specific targets and numerous cognitive improvements. This review focuses on the different models of global cerebral ischemia, neuronal synaptic alterations, synaptic neuroprotection and behavioral tests that can be used to determine deficits in cognitive function after global cerebral ischemia.
Keywords: Aging, cardiac arrest, global cerebral ischemia, hippocampus, neuroprotection, synapse
Current Drug Targets
Title:Global Cerebral Ischemia: Synaptic and Cognitive Dysfunction
Volume: 14 Issue: 1
Author(s): Jake T. Neumann, Charles H. Cohan, Kunjan R. Dave, Clinton B. Wright and Miguel A. Perez-Pinzon
Affiliation:
Keywords: Aging, cardiac arrest, global cerebral ischemia, hippocampus, neuroprotection, synapse
Abstract: Cardiopulmonary arrest is one of the leading causes of death and disability, primarily occurring in the aged population. Numerous global cerebral ischemia animal models induce neuronal damage similar to cardiac arrest. These global cerebral ischemia models range from vessel occlusion to total cessation of cardiac function, both of which have allowed for the investigation of this multifaceted disease and detection of numerous agents that are neuroprotective. Synapses endure a variety of alterations after global cerebral ischemia from the resulting excitotoxicity and have been a major target for neuroprotection; however, neuroprotective agents have proven unsuccessful in clinical trials, as neurological outcomes have not displayed significant improvements in patients. A majority of these neuroprotective agents have specific neuronal targets, where the success of future neuroprotective agents may depend on non-specific targets and numerous cognitive improvements. This review focuses on the different models of global cerebral ischemia, neuronal synaptic alterations, synaptic neuroprotection and behavioral tests that can be used to determine deficits in cognitive function after global cerebral ischemia.
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Cite this article as:
T. Neumann Jake, H. Cohan Charles, R. Dave Kunjan, B. Wright Clinton and A. Perez-Pinzon Miguel, Global Cerebral Ischemia: Synaptic and Cognitive Dysfunction, Current Drug Targets 2013; 14 (1) . https://dx.doi.org/10.2174/1389450111314010004
DOI https://dx.doi.org/10.2174/1389450111314010004 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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