Abstract
In ischemic stroke, apoptosis persists for days to weeks after the onset of an ischemic event. Cysteine-ASPartic proteASEs (caspases) are key mediators of apoptosis and neurodegeneration in stroke. The impact of caspase activity is not restricted to neuronal death, as caspases can exacerbate inflammation and alter glial function. Thus, caspases are logical therapeutic targets for this disease, but they have never been clinically evaluated due to a paucity of ideal drug candidates. Recent developments in caspase inhibition and drug delivery offer novel neuroprotective strategies for stroke, which are deliberated in this review.