Global Cerebral Ischemia: Synaptic and Cognitive Dysfunction
Jake T. Neumann, Charles H. Cohan, Kunjan R. Dave, Clinton B. Wright and Miguel A. Perez-Pinzon
Affiliation: Department of Neurology D4- 5, University of Miami Miller School Of Medicine, PO Box 016960, Miami, FL 33101, USA.
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
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