Individual Neuronal Apoptosis Provokes Determined Necrosis of the Regional Cerebral Infarct in Patients with Ischemic Stroke

Stroke patients comprise a large number of patients with a highly significant degree of cerebral ischemia that is best exemplified by the transient focal ischemia models in experimental animals such as rat and mouse. Mechanisms include bioenergetic failure and loss of cell homeostasis, and also acidosis, excitotoxicity and disrupted blood-brain barrier [1]. A central issue is the series of set conditioning factors that induce apoptosis of individual neurons within the penumbral region of the cerebral cortex on the one hand and the development if neuronal necrosis on the other. Combined steroid administration inhibits ischemia-induced apoptosis of neutrons through involvement of the intrinsic pathways [2]. It would appear that a combination of both apoptosis and necrosis of neurons evolves in at least some of the patients, and indeed neurons may exhibit features of both these forms of neuronal cell death when electron microscopic studies are combined with molecular and biochemical modes of analysis. Whether necrosis or apoptosis occurs often depends on cell type, cell age and location in the brain. Apoptosis leader to protein crosslinking, DNA fragmentation, ligand expression for phagocytic cell receptors and subsequent phagocytic uptake [3].