Dr. Denson Fujikawa is an Adjunct Professor of Neurology at the David Geffen School of Medicine at UCLA, a member of the Brain Research Institute at UCLA and a Staff Neurologist at the Department of Veterans Affairs Greater Los Angeles Healthcare System. His interest in mechanisms of nerve cell death in the brain began during a two-year epilepsy research fellowship with Dr. Claude Wasterlain, from 1981 to 1983. He is a Fellow of the American Academy of Neurology and is a member of the American Epilepsy Society, American Neurological Association, International Society for Cerebral Blood Flow and Metabolism and the Society for Neuroscience.

• 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.

Dr. Denson Fujikawa is an Adjunct Professor of Neurology at the David Geffen School of Medicine at UCLA, a member of the Brain Research Institute at UCLA and a Staff Neurologist at the Department of Veterans Affairs Greater Los Angeles Healthcare System. His interest in mechanisms of nerve cell death in the brain began during a two-year epilepsy research fellowship with Dr. Claude Wasterlain, from 1981 to 1983. He is a Fellow of the American Academy of Neurology and is a member of the American Epilepsy Society, American Neurological Association, International Society for Cerebral Blood Flow and Metabolism and the Society for Neuroscience.

• 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.

Dr. Denson Fujikawa is an Adjunct Professor of Neurology at the David Geffen School of Medicine at UCLA, a member of the Brain Research Institute at UCLA and a Staff Neurologist at the Department of Veterans Affairs Greater Los Angeles Healthcare System. His interest in mechanisms of nerve cell death in the brain began during a two-year epilepsy research fellowship with Dr. Claude Wasterlain, from 1981 to 1983. He is a Fellow of the American Academy of Neurology and is a member of the American Epilepsy Society, American Neurological Association, International Society for Cerebral Blood Flow and Metabolism and the Society for Neuroscience.

• 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.