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Titlebook: Excitotoxicity in Neurological Diseases; New Therapeutic Chal Carlo Ferrarese,M. Flint Beal Book 2004 Springer Science+Business Media New Y

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發(fā)表于 2025-3-21 17:14:18 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Excitotoxicity in Neurological Diseases
副標(biāo)題New Therapeutic Chal
編輯Carlo Ferrarese,M. Flint Beal
視頻videohttp://file.papertrans.cn/319/318415/318415.mp4
圖書封面Titlebook: Excitotoxicity in Neurological Diseases; New Therapeutic Chal Carlo Ferrarese,M. Flint Beal Book 2004 Springer Science+Business Media New Y
描述It can be reasonably anticipated that, over the next generations, the proportion of elderly people will remarkably increase and, with this, the number ofpersons suffering from acute (e.g. cerebral ischemia) or chronic neurodegenerative disorders. To date, approved drugs only alleviate the symptoms ofthese diseases (for instance, acetylcholinesterase inhibitors in Alzheimer disease and L-dopa and dopamine-agonists in Parkinson disease), while none seems to stop the progression of the degenerative processes underlying them. The development of effective preventive or protective therapies has been impeded by the limitations of our knowledge of the causes and the mechanisms by which neurons die in neurodegenerative disorders. Evidence accumulated in the past 20 years indicated that the major excitatory neurotransmitter glutamate may play a role as neurotoxin in several conditions. In particular, the glutamatergic system dysfunction seems to be an early event working as a common pathway in the pathogenesis ofa large number ofacute and chronic neurological disorders, in strict conjunction with other important mechanisms, such as oxidative stress and energetic failure, and probably trigger
出版日期Book 2004
關(guān)鍵詞Alzheimer; Parkinson; alzheimer‘s disease; brain; brain injury; cerebral ischemia; dementia; glutamate rece
版次1
doihttps://doi.org/10.1007/978-1-4419-8959-8
isbn_softcover978-1-4613-4736-1
isbn_ebook978-1-4419-8959-8
copyrightSpringer Science+Business Media New York 2004
The information of publication is updating

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Contribution of Astrocyte Glutamate Release to Excitotoxicityreceptors and are able to release transmitters by regulated pathways. Astrocytes were found to react to synaptically released neurotransmitters by undergoing intracellular calcium elevation which subsequently triggers an exocytosis-like glial transmitter release. These findings led to a new concept
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Metabotropic Glutamate Receptors and Neurodegenerationneuroprotective drugs and the advent of potent and centrally available subtype-selective ligands has lead to an extensive investigation of the role of individual mGlu receptor subtypes in neurodegeneration. Pharmacological blockade of mGlu1 or -5 receptors or pharmacological activation of mGlu2/3 or
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Epilepsy and Seizures: Excitotoxicity or Excitotrophicity? that may last for hours. The severity and duration of SE determine the extent of neuronal injury; in most animal models damage is observed with durations of one hour or longer. Severity, duration and rate of onset may also influence the extent to which the neuronal death is mediated by apoptotic or
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Excitotoxicity in Cerebral Ischemiauding the neuroprotective activity of glutamate receptor antagonists in experimental animal models and the use of anti-excitotoxic agents in clinical trials for stroke. Despite the dramatic results in the preclinical setting, phase III clinical trials with neuroprotective drugs have been generally u
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Excitotoxicity and Traumatic Brain Injury consequences. Despite numerous clinical trials investigating pharmaceutical compounds with promising pre-clinical efficacy, no pharmacological treatment has been developed with proven clinical efficacy. The present chapter reviews the pathophysiology of TBI with focus on the evidence of and mechani
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