New PDF release: Acute Neuronal Injury: The Role of Excitotoxic Programmed

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

ISBN-10: 038773225X

ISBN-13: 9780387732251

This publication is the results of a convergence of medical information about mechanisms that produce acute nerve mobilephone demise within the mind. even though doubtless 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 particular subtype of glutamate receptor by means of 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 a number of enzymes which are accountable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve mobilephone loss of life. The excessive calcium focus additionally interferes with mitochondrial breathing, with the ensuing construction of loose radicals that harm mobile membranes and nuclear DNA. figuring out the biochemical pathways that produce nerve cellphone dying is step one towards devising a good neuroprotective process, the final word goal.

Acute Neuronal damage may be valuable to neuroscientists and common cellphone biologists attracted to mobile loss of life. The booklet can be worthy 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 college 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 procedure. His curiosity in mechanisms of nerve telephone demise within the mind started in the course of a two-year epilepsy study 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 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

As indicated above, AIF release from mitochondria occurs in a number of cell types, independently of the nature of the death-triggering signal (Kim et al. 2003a; Murahashi et al. 2003; Zhu et al. 2003). The requirement of nuclear translocation for AIF-mediated induction of caspase-independent, apoptosis-like PCD has been explicitly demonstrated by microinjection experiments of AIF-directed antibodies, which potently inhibited AIF targeting to the nucleus as well as cell 42 S. A. Susin death (Susin et al.

Elegans indicate that specific molecular mechanisms are involved in the necrotic destruction of the cell. Because necrosis is implicated in many devastating human disorders, such as neurodegenerative diseases and stroke, elucidation of the biochemical events that transpire during necrosis has the potential to provide targets for effective pharmacological interventions. In addition to the three major categories of caspase-independent cell death, novel cell death paradigms that do not involve caspase function are emerging.

Proc Natl Acad Sci USA 103:11573–11578 Murakami S (2007) Caenorhabditis elegans as a model system to study aging of learning and memory. Mol Neurobiol 35:85–94 Nakano Y, Fujitani K, Kurihara J, Ragan J, Usui-Aoki K, Shimoda L, Lukacsovich T, Suzuki K, Sezaki M, Sano Y, Ueda R, Awano W, Kaneda M, Umeda M, Yamamoto D (2001) Mutations in the novel membrane protein spinster interfere with programmed cell death and cause neural degeneration in Drosophila melanogaster. Mol Cell Biol 21:3775–3788 Nass R, Hall DH, Miller DM 3rd, Blakely RD (2002) Neurotoxin-induced degeneration of dopamine neurons in Caenorhabditis elegans.

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Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms by Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)


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