Current Drug Targets

Francis J. Castellino
Kleiderer-Pezold Professor of Biochemistry
Director, W.M. Keck Center for Transgene Research
Dean Emeritus, College of Science
230 Raclin-Carmichael Hall, University of Notre Dame
Notre Dame, IN 46556


Global Cerebral Ischemia: Synaptic and Cognitive Dysfunction

Author(s): 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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Article Details

Page: [20 - 35]
Pages: 16
DOI: 10.2174/1389450111314010004