Download e-book for kindle: Acute Neuronal Injury: The Role of Excitotoxic Programmed by Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)

By Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)

ISBN-10: 038773225X

ISBN-13: 9780387732251

This e-book is the results of a convergence of clinical information about mechanisms that produce acute nerve cellphone loss of life within the mind. even supposing probably disparate, stroke, mind and spinal twine 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 via an increased extracellular glutamate focus that ends up in an over the top inflow of calcium into nerve cells. The excessive calcium focus in nerve cells prompts numerous enzymes which are chargeable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve phone dying. The excessive calcium focus additionally interferes with mitochondrial breathing, with the consequent creation of loose radicals that harm mobile membranes and nuclear DNA. figuring out the biochemical pathways that produce nerve phone demise is step one towards devising a good neuroprotective method, the final word goal.

Acute Neuronal harm may be valuable to neuroscientists and basic telephone biologists attracted to cellphone dying. The e-book may also be important 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 university of medication at UCLA, a member of the mind study Institute at UCLA and a employees Neurologist on the division of Veterans Affairs better la Healthcare approach. His curiosity in mechanisms of nerve mobile loss of life within the mind all started in the course of a two-year epilepsy learn 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 yank Epilepsy Society, American Neurological organization, overseas Society for Cerebral Blood movement 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

Sample text

TAIF then translocates from mitochondria to cytosol and further to the nucleus, where it interacts with DNA and causes caspase-independent chromatin condensation and participates in large-scale (~50 kb) DNA fragmentation (Susin et al. 1999; Ye et al. 2002). The mitochondrial release, nuclear translocation, and DNA fragmentation associated with AIF have now been extensively demonstrated in several cell death systems and cell types (~900 references in Medline to date). Three additional AIF isoforms have been characterized (1) AIF-exB, generated by an alternative use of exon 2b (rather than exon 2) (Loeffler et al.

These cytoplasmic vesicles contain cellular organelles, such as mitochondria or endoplasmic reticulum (Gozuacik and Kimchi 2007). It is important to distinguish “autophagic death” from autophagy. Indeed, autophagy is an adaptive process involved in survival response to low-nutrient states (in hypoglycemia, after axonal injury, etc), allowing for the catabolism of cellular constituents to produce energy or to remove damaged organelles. However, autophagy is also associated with cell death with either necrotic or apoptotic phenotype [for review, see Nixon (2006)].

Mol Cell 11:987–996 Parrish J, Li L, Klotz K, Ledwich D, Wang X, Xue D (2001) Mitochondrial endonuclease G is important for apoptosis in C. elegans. Nature 412:90–94 Parrish JZ, Yang C, Shen B, Xue D (2003) CRN-1, a Caenorhabditis elegans FEN-1 homologue, cooperates with CPS-6/EndoG to promote apoptotic DNA degradation. EMBO J 22:3451–3460 Porter AG, Urbano AG (2006) Does apoptosis-inducing factor (AIF) have both life and death functions in cells? Bioessays 28:834–843 Ravikumar B, Vacher C, Berger Z, Davies JE, Luo S, Oroz LG, Scaravilli F, Easton DF, Duden R, O’Kane CJ, Rubinsztein DC (2004) Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease.

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