Abstract

The quest to understand the neurobiology of ischemic brain injury has relied on the investigational techniques available over the years. Historically, morbid anatomy was the approach used through the midportion of the last century.1 The establishment of the Journal of Neurochemisty in 1956 marks the assent of tools to understanding brain injury beyond the whole organ level. Cellular and molecular approaches supervened especially after the discovery of apoptosis or programmed cell death by Kerr and colleagues in 1972,2 which lead to a focus on cellular and molecular cell death mechanisms. We now know that ischemic cell death is accompanied by transcriptional and translational events that may modulate ischemic injury. The induction of death-inducing gene products, such as the caspases, and the regulation of prosurvival gene products, such as antiapoptotic bcl-2 family genes, are now well known.3 More broad-based approaches to gene modulation in disease, such as …

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