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.)

This ebook is the results of a convergence of clinical information about mechanisms that produce acute nerve mobilephone 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 particular 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 a number of enzymes which are answerable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve mobile dying. The excessive calcium focus additionally interferes with mitochondrial respiratory, with the ensuing construction of loose radicals that harm mobile membranes and nuclear DNA. figuring out the biochemical pathways that produce nerve phone dying is step one towards devising a good neuroprotective technique, the last word goal.

Acute Neuronal harm should be worthy to neuroscientists and basic phone biologists attracted to mobile demise. The e-book can also 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 institution of drugs at UCLA, a member of the mind learn Institute at UCLA and a employees Neurologist on the division of Veterans Affairs larger l. a. Healthcare procedure. His curiosity in mechanisms of nerve mobilephone dying within the mind all 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 move and Metabolism, and the Society for Neuroscience.

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Detailed studies of cell death following brain ischemia in monkeys have led to the formulation of the “calpain–cathepsin” hypothesis for the execution of necrosis (Yamashima 2000, 2004). Genetic studies in C. elegans support the involvement of a calpain–cathepsin axis during neurodegeneration. Downregulation of the calpains CLP-1 and TRA-3 and cathepsins ASP-3 and ASP-4 by RNAi ameliorates neurodegeneration in the nematode (Syntichaki et al. 2002). The proteolytic action of cathepsins in the cytoplasm is further enhanced by the drop of pH in the cell, mediated by the vacuolar H+ATPase, which acidifies lysosomes and other cell organelles.

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