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Description
An overview of the biochemical mechanisms that produce acute nerve cell death in the brain. Covers injuries and disorders including stroke, brain and spinal cord trauma, hypoglycemic coma, and prolonged epileptic seizures. All of these lead to high concentrations of calcium in nerve cells which, in turn, causes degradation of cytoplasmic proteins, cleavage of nuclear DNA, and eventually cell death.
Table of Contents
Introduction.- Excitotoxic programmed cell death involves caspase-independent mechanisms.- To survive or to die: how neurons deal with it.- Oxidative damage mechanisms in traumatic brain injury and antioxidant neuroprotective approaches.- Mitochondrial damage in traumatic CNS injury.- Neuroprotective agents target molecular mechanisms of programmed cell death after traumatic brain injury.- Involvement of apoptosis-inducing factor (AIF) in neuronal death following cerebral ischemia.- Apoptosis-inducing factor translocation to nuclei after transient global ischemia.- Necroptosis in cerebral ischemia.- Histological and elemental changes in ischemic stroke.- Hypoglycemic brain damage.- Activation of caspase-independent programmed pathways in seizure-induced neuronal necrosis.- Conclusion.
