Scientists in the field of stroke research have defined multiple pathways that mediate stroke-induced cell death. Experimentally, the mechanisms underlying neuronal death are often elucidated through the use of small molecule agonists and inhibitors. For example, small molecules may reveal whether cell death is mediated by caspase-dependent apoptosis or through a caspase-independent pathway such as necrosis. Similar strategies can be used to define signaling pathways that mediate ischemia-induced damage such as the breakdown of endothelial tight junctions in the blood-brain barrier (BBB).
The results obtained using small molecule experimental approaches continue to advance our understanding of the pathways that underlie stroke-related cell death. Further elucidation of the molecular mechanisms involved may reveal potential drug targets for stroke treatment. Such findings are not only relevant to stroke research but also to related fields. For example, advances in understanding the regulation of BBB permeability are important to the field of drug development and delivery since the BBB poses a significant obstacle in the development of drugs used to treat neurological conditions. Similarly, findings in the area of apoptosis or oxidative stress are relevant to many non-neurological conditions such as diabetes and atherosclerosis.