Abstract
Brain ischemia resulting from multiple disease states including cardiac arrest, stroke and traumatic brain injury, is a leading cause of death and disability. Despite significant resources dedicated to developing pharmacological interventions, few effective therapeutic options are currently available. The basic consequence of cerebral ischemia, characterized by energy failure and subsequent brain metabolic abnormalities, enables the protective effects by pharmacological manipulation of brain metabolism. We present here the important roles of brain glycogen metabolism and propose inhibition of glycogenolysis as a therapeutic approach to cerebral ischemia.
Keywords: Brain glycogen, cerebral ischemia, glycogenolysis, inhibitors, Brain ischemia, traumatic brain injury, brain glycogen metabolism, Brain, Neurons, glycogen synthase, Astrocytes, neurotransmitters, glycogen phosphorylase, phosphorylase kinase, glucose-6-phosphate, hypoglycemia, oxidative phosphorylation, glutamate mediated excitotox-icity, Glycogen Storage, methinionine sulfoximine, glucose-depleted brain tissue, glutathione system, Glutathione disulfide, Amelioration of Lactic Acidosis, glycolytic pathway, glycolytic substrate, Mitochondria, reactive oxygen species, Maslinic Acid, CP-316819, Magnesium Sulfate, N-methyl-D-aspartate, Uridine diphosphate glucose, uridine triphos-phate, glucose-1-phosphate uridyltrans-ferase, electroencephalogram
Mini-Reviews in Medicinal Chemistry
Title: Pharmacological Manipulation of Brain Glycogenolysis as a Therapeutic Approach to Cerebral Ischemia
Volume: 10 Issue: 12
Author(s): L. Xu and H. Sun
Affiliation:
Keywords: Brain glycogen, cerebral ischemia, glycogenolysis, inhibitors, Brain ischemia, traumatic brain injury, brain glycogen metabolism, Brain, Neurons, glycogen synthase, Astrocytes, neurotransmitters, glycogen phosphorylase, phosphorylase kinase, glucose-6-phosphate, hypoglycemia, oxidative phosphorylation, glutamate mediated excitotox-icity, Glycogen Storage, methinionine sulfoximine, glucose-depleted brain tissue, glutathione system, Glutathione disulfide, Amelioration of Lactic Acidosis, glycolytic pathway, glycolytic substrate, Mitochondria, reactive oxygen species, Maslinic Acid, CP-316819, Magnesium Sulfate, N-methyl-D-aspartate, Uridine diphosphate glucose, uridine triphos-phate, glucose-1-phosphate uridyltrans-ferase, electroencephalogram
Abstract: Brain ischemia resulting from multiple disease states including cardiac arrest, stroke and traumatic brain injury, is a leading cause of death and disability. Despite significant resources dedicated to developing pharmacological interventions, few effective therapeutic options are currently available. The basic consequence of cerebral ischemia, characterized by energy failure and subsequent brain metabolic abnormalities, enables the protective effects by pharmacological manipulation of brain metabolism. We present here the important roles of brain glycogen metabolism and propose inhibition of glycogenolysis as a therapeutic approach to cerebral ischemia.
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Cite this article as:
Xu L. and Sun H., Pharmacological Manipulation of Brain Glycogenolysis as a Therapeutic Approach to Cerebral Ischemia, Mini-Reviews in Medicinal Chemistry 2010; 10 (12) . https://dx.doi.org/10.2174/1389557511009011188
DOI https://dx.doi.org/10.2174/1389557511009011188 |
Print ISSN 1389-5575 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5607 |
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