Cell Death Pathways

Inhibition of apoptosis is repeatedly proposed as a novel and promising therapeutic direction for attempts at cell rescue following stroke. In that the immature brain undergoes programmed cell death to ensure normal brain development, the effects of inhibiting this program must be considered when developing therapies. Cell death in the injured developing brain has been termed "neuronal necrosis" or "excitotoxic neurodegeneration" (43). It has been argued that true apoptosis occurs only in a second wave of cell death following neonatal hypoxic-ischemic brain injury as a consequence of target deprivation (44-47). However, the cell death may actually represent a "continuum" phenotype that incorporates features of both (48). Recent commentaries point to the controversy surrounding the classification of developmental cell death phenotypes (49,50) . The strongest biochemical evidence for the presence of an intermediate continuum form of cell death is outlined in a recent study in which markers for both apoptosis and necrosis are demonstrated in injured forebrain neurons early following neonatal hypoxic-ischemic brain injury (51). Inhibition by apoptosis inhibitors provides only partial protection, further supporting these anatomic data (52). In the reperfusion model of neonatal stroke, classic markers for activation of apoptotic pathways fail to coincide with the severity of injury, suggesting a role for necrosis as well (53).

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