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Review Article Open Access
Over the past two decades, research has heavily emphasized basic mechanisms that irreversibly damage brain cells after stroke. Much attention has focused on what makes neurons die easily and what strategies render neurons resistant to ischaemic injury. In the past few years, clinical experience with clot-lysing drugs has confirmed expectations that early reperfusion improves clinical outcome.Although great advances have been made in understanding the diverse mechanisms of neuronal cell death induced by ischemic stroke, clinically effective neuroprotective therapies are limited.Based on the accumulating evidence that ischemic cell death is a result of series of subsequent biochemical events, new concepts for prevention and treatment of ischemic stroke may eventually emerge without the hazard of severe complications.This review focuses on mechanisms and emerging concepts that drive the science of ischemic stroke in a therapeutic direction. Once considered exclusively a disorder of blood vessels, growing evidence has led to the realization that the biological processes underlying stroke are driven by the interaction of neurons, glia, vascular cells and matrix components, which actively participate in mechanisms of tissue injury and repair. As new targets are identified, new opportunities emerge that build on an appreciation of acute cellular events acting in a broader context of ongoing destructive, protective and reparative processes. This review then poses a number of fundamental questions, the answers to which may generate a number of treatment strategies and possibly new treatments that could reduce the impact of this enormous economic and societal burden.
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Author(s): Neema Kanyal
Apoptosis, excitotoxicity, ischemia, stroke, Apoptosis, excitotoxicity, ischemia, stroke