Several complex and overlapping pathways underlie the pathophysiology of cell death after ischemic stoke. While pharmaceutical agents can inhibit these pathways at various levels, resulting in effective neuroprotection in experimental models, no single agent intended for neuroprotection has been shown to improve outcome in clinical stroke trials. Refinements in patient selection, brain imaging, and methods of drug delivery, as well as the use of more clinically relevant animal stroke models and use of combination therapies that target the entire neurovascular unit are warranted to make stroke neuroprotection an achievable goal. Ongoing trials assessing the efficacy of thrombolysis with neuroprotective agents, and strategies aimed at extending the therapeutic window for reperfusion therapy promise to enhance the known benefits of reperfusion therapy. Most investigators agree that genomics and proteomics are the most promising recent developments impacting the future of stroke prevention, diagnosis, treatment, and outcome. Although many challenges lie ahead, an attitude of cautious optimism seems justified at this time.

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