Gene expression after cerebral ischemia

Global and focal ischemias induce a variety of gene families, including immediate early genes, cytokines, neurotransmitter receptors, and heat-shock proteins. The Janus-like effects of several of these gene products promote neuronal survival and degeneration. Therefore, determining the molecular pathways responsible for the differential regulation of these genes is of paramount importance. The discovery of apoptosis as a mediator of delayed neuronal death has led to the identification of a number of other genes involved in postischemic brain damage. Future neuroprotective therapies for cerebral ischemia may be directed at preventing alterations in gene expression.