Acute Neuronal Injury

The Role of Excitotoxic Programmed Cell Death Mechanisms

Inbunden, Engelska, 2018

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An overview of the biochemical mechanisms that produce acute nerve cell death in the brain. 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.

Produktinformation

Utgivningsdatum2018-09-19
Mått155 x 235 x 18 mm
Vikt512 g
FormatInbunden
SpråkEngelska
Antal sidor215
Upplaga2
FörlagSpringer International Publishing AG
ISBN9783319774947

Tillhör följande kategorier

Psykiatri inom Medicin
Biovetenskap inom Naturvetenskap och teknik
Cellbiologi inom Naturvetenskap och teknik
Neurologi och klinisk neurofysiologi inom Medicin
Patologi inom Medicin

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.