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10.1038/aps.2009.24

http://scihub22266oqcxt.onion/10.1038/aps.2009.24
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suck abstract from ncbi


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pmid19343058      Acta+Pharmacol+Sin 2009 ; 30 (4): 379-87
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  • Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases #MMPMID19343058
  • Dong XX; Wang Y; Qin ZH
  • Acta Pharmacol Sin 2009[Apr]; 30 (4): 379-87 PMID19343058show ga
  • A pivotal role for excitotoxicity in neurodegenerative diseases is gaining increasingly more acceptance, but the underlying mechanisms through which it participates in neurodegeneration still need further investigation. Excessive activation of glutamate receptors by excitatory amino acids leads to a number of deleterious consequences, including impairment of calcium buffering, generation of free radicals, activation of the mitochondrial permeability transition and secondary excitotoxicity. Recent studies implicate excitotoxicity in a variety of neuropathological conditions, suggesting that neurodegenerative diseases with distinct genetic etiologies may share excitotoxicity as a common pathogenic pathway. Thus, understanding the pathways involved in excitotoxicity is of critical importance for the future clinical treatment of many neurodegenerative diseases. This review discusses the current understanding of excitotoxic mechanisms and how they are involved in the pathogenesis of neurodegenerative diseases.
  • |Alzheimer Disease/etiology[MESH]
  • |Animals[MESH]
  • |Apoptosis[MESH]
  • |Autophagy[MESH]
  • |Calcium/metabolism[MESH]
  • |Chlorides/metabolism[MESH]
  • |Glutamic Acid/*toxicity[MESH]
  • |Humans[MESH]
  • |Huntington Disease/etiology[MESH]
  • |Neurodegenerative Diseases/etiology[MESH]
  • |Nitric Oxide/physiology[MESH]
  • |Oxidative Stress[MESH]
  • |Reactive Oxygen Species/metabolism[MESH]
  • |Receptors, AMPA/physiology[MESH]
  • |Receptors, Glutamate/physiology[MESH]


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