By Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)
This publication is the results of a convergence of medical information about mechanisms that produce acute nerve mobile demise within the mind. even supposing possible disparate, stroke, mind and spinal wire trauma, coma from a low serum glucose focus (hypoglycemia), and lengthy epileptic seizures have in universal the inciting issue of excitotoxicity, the activation of a selected subtype of glutamate receptor by way of an increased extracellular glutamate focus that leads to an over the top inflow of calcium into nerve cells. The excessive calcium focus in nerve cells prompts a number of enzymes which are chargeable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve telephone dying. The excessive calcium focus additionally interferes with mitochondrial respiratory, with the ensuing construction of unfastened radicals that harm mobile membranes and nuclear DNA. figuring out the biochemical pathways that produce nerve telephone dying is step one towards devising a good neuroprotective technique, the last word goal.
Acute Neuronal harm may be priceless to neuroscientists and basic telephone biologists drawn to telephone demise. The booklet can also be priceless to clinically orientated neuroscientists, together with neurologists, neurosurgeons and psychiatrists.
About the Editor:
Dr. Denson Fujikawa is an accessory Professor of Neurology on the David Geffen tuition of medication at UCLA, a member of the mind examine Institute at UCLA and a employees Neurologist on the division of Veterans Affairs larger la Healthcare procedure. His curiosity in mechanisms of nerve telephone dying within the mind begun in the course of a two-year epilepsy examine fellowship with Dr. Claude Wasterlain, from 1981 to 1983. he's a Fellow of the yankee Academy of Neurology and is a member of the yankee Epilepsy Society, American Neurological organization, foreign Society for Cerebral Blood circulate and Metabolism, and the Society for Neuroscience.
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Additional resources for Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms
38 S. A. Susin Apoptosis-like PCD occurs through a caspase-independent mitochondrial route. Apoptosis-inducing factor (AIF) is currently considered the major apoptosis-like PCD effector (Krantic et al. 2007; Susin et al. 1996, 1997, 1999, 2000; Boujrad et al. 2007; Lorenzo and Susin 2007; Dawson and Dawson 2004; Yu et al. 2002; Hong et al. 2004). Upon MOMP, AIF is released from the intermembrane mitochondrial space. The kinetics of AIF release is, however, slower than that of cytochrome c release (Munoz-Pinedo et al.
Development 130:5779–5789 30 M. Rieckher and N. Tavernarakis Miramar MD, Costantini P, Ravagnan L, Saraiva LM, Haouzi D, Brothers G, Penninger JM, Peleato ML, Kroemer G, Susin SA (2001) NADH oxidase activity of mitochondrial apoptosisinducing factor. J Biol Chem 276:16391–16398 Modjtahedi N, Giordanetto F, Madeo F, Kroemer G (2006) Apoptosis-inducing factor: vital and lethal. Trends Cell Biol 16:264–272 Munoz-Pinedo C, Guio-Carrion A, Goldstein JC, Fitzgerald P, Newmeyer DD, Green DR (2006) Different mitochondrial intermembrane space proteins are released during apoptosis in a manner that is coordinately initiated but can vary in duration.
Nature 417:851–854 Brand AH, Perrimon N (1993) Targeted gene expression as a means of altering cell fates and generating dominant phenotypes. Development 118:401–415 Brenner S (1974) The genetics of Caenorhabditis elegans. Genetics 77:71–94 Broker LE, Kruyt FA, Giaccone G (2005) Cell death independent of caspases: a review. Clin Cancer Res 11:3155–3162 Carthew RW (2007) Pattern formation in the Drosophila eye. Curr Opin Genet Dev 17:309–313 Cauchi RJ, van den Heuvel M (2006) The fly as a model for neurodegenerative diseases: is it worth the jump?