Unfortunately, current stroke therapies approved for human use are very limited. The only drug clinically available in the US is intravenous recombinant tissue plasminogen activator (rt-PA), a thrombolytic agent that has been shown to improve stroke patient functional outcomes. However, rt-PA is only effective if administered within the first 3 hours after symptom onset and carries with it a significant risk of intracranial hemorrhage. Consequently, only about 5 to 10% of patients can receive this therapy. Over 1,000 other potential stroke therapeutics have been tested in preclinical cerebral stroke models and approximately one tenth of these have made it to clinical trials. However, the majority of these efforts have already failed. It is likely that the most effective way to improve outcomes is rapid reperfusion of the ischemic area using thrombolytic means in combination with neuroprotective strategies to salvage cells within the penumbra and prevent them from becoming part of the ischemic core. To this end, researchers have been increasingly focused on post-stroke neuroinflammation and the role it plays in neurotoxicity and neuroprotection. [1-4]
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Ceulemans, A.-G., Zgavc, T., Kooijman, R., Hachimi-Idrissi, S., Sarre, S., and Michotte, Y. (2010). The dual role of the neuroinflammatory response after ischemic stroke: modulatory effects of hypothermia. Journal of Neuroinflammation 7:74.
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