標(biāo)題: Titlebook: Excitotoxicity in Neurological Diseases; New Therapeutic Chal Carlo Ferrarese,M. Flint Beal Book 2004 Springer Science+Business Media New Y [打印本頁] 作者: 強(qiáng)烈的愿望 時(shí)間: 2025-3-21 17:14
書目名稱Excitotoxicity in Neurological Diseases影響因子(影響力)
書目名稱Excitotoxicity in Neurological Diseases影響因子(影響力)學(xué)科排名
書目名稱Excitotoxicity in Neurological Diseases網(wǎng)絡(luò)公開度
書目名稱Excitotoxicity in Neurological Diseases網(wǎng)絡(luò)公開度學(xué)科排名
書目名稱Excitotoxicity in Neurological Diseases被引頻次
書目名稱Excitotoxicity in Neurological Diseases被引頻次學(xué)科排名
書目名稱Excitotoxicity in Neurological Diseases年度引用
書目名稱Excitotoxicity in Neurological Diseases年度引用學(xué)科排名
書目名稱Excitotoxicity in Neurological Diseases讀者反饋
書目名稱Excitotoxicity in Neurological Diseases讀者反饋學(xué)科排名
作者: 混雜人 時(shí)間: 2025-3-21 23:15
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 作者: ALE 時(shí)間: 2025-3-22 00:49 作者: 易改變 時(shí)間: 2025-3-22 08:01 作者: CRUE 時(shí)間: 2025-3-22 08:54 作者: –scent 時(shí)間: 2025-3-22 16:37
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作者: –scent 時(shí)間: 2025-3-22 19:05 作者: 懶洋洋 時(shí)間: 2025-3-23 00:06
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作者: 評論性 時(shí)間: 2025-3-23 03:26
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作者: –DOX 時(shí)間: 2025-3-23 06:29
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作者: 熱心 時(shí)間: 2025-3-23 12:18 作者: lactic 時(shí)間: 2025-3-23 14:52 作者: 沖擊力 時(shí)間: 2025-3-23 19:03
Excitotoxicity in Huntington’s Diseasele was developed after the observation that kainic acid induced striatal lesions which mimic many of the neuropathologic features of HD. We and others subsequently showed that quinolinic acid lesions, which spare NADPH-diaphorase neurons, produced an improved excitotoxic model. There however is no e作者: FLEET 時(shí)間: 2025-3-24 02:12
The Glutamatergic System in Alzheimer’s Disease Brain: Dysfunction Associated with Amyloid β-Peptidest in brain. However, in Alzheimer’s disease (AD) brain, the glutamate transporter and glutamine synthestase function with considerably reduced activity. Consistent with the observed oxidative stress in AD brain and the oxidative stress induced by amyloid β-peptide (Aβ), both the glutamate transport作者: Jocose 時(shí)間: 2025-3-24 04:32
Neurotoxicity and Prion Diseasested to be both the infectious agent and the cause of neuronal cell death in the disease. Death of the patient results from neurodegeneration. In this review, we present data arguing that neurodegeneration in prion diseases is a complex process, involving the action of other factors in addition to t作者: alliance 時(shí)間: 2025-3-24 06:35 作者: Precursor 時(shí)間: 2025-3-24 10:45
HIV-1 associated dementiauropathology remains incompletely understood, several lines of evidence suggest the involvement of chemokine receptors, inflammatory factors and NMDA receptor-mediated excitotoxicity. All of these can in tum trigger several downstream mechanisms, including excessive influx of Ca. ions, activation of作者: TAIN 時(shí)間: 2025-3-24 16:12
Book 2004ar, 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作者: Manifest 時(shí)間: 2025-3-24 21:32
n 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 trigger978-1-4613-4736-1978-1-4419-8959-8作者: 嫻熟 時(shí)間: 2025-3-25 01:20 作者: 窗簾等 時(shí)間: 2025-3-25 03:57 作者: creditor 時(shí)間: 2025-3-25 09:32
Metabotropic Glutamate Receptors and Neurodegenerationential application of mGlu5 receptor antagonists in chronic neurodegenerative disorders, such as Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s disease (AD). MGlu2/3 receptor agonists inhibit glutamate release, and also promote the synthesis and release of neurotrophic factors in astrocytes. Th作者: 含糊其辭 時(shí)間: 2025-3-25 15:12
Mechanisms of Excitotoxicity and Excitoprotection such as caspase-3. Essentially all subcellular compartments, including the endoplasmic reticulum, mitochondria and nucleus are involved in the excitotoxic process. Excitotoxic cascades are initiated in postsynaptic dendrites where glutamate receptors are most highly concentrated, and may either cau作者: 多嘴 時(shí)間: 2025-3-25 17:18 作者: 地牢 時(shí)間: 2025-3-25 21:36 作者: certain 時(shí)間: 2025-3-26 02:54 作者: 無孔 時(shí)間: 2025-3-26 07:36
Glutamate Transmission in the Pathogenesis of Parkinson’s Diseasenuclein and parkin. Moreover, compelling evidence supports the involvement of mitochondrial metabolism failure as an essential cofactor in the pathogenesis of PD. Interestingly, some environmental toxins are thought to be able to act as mitochondrial toxins. The comprehension of the pathways leading作者: Ointment 時(shí)間: 2025-3-26 10:45 作者: 門窗的側(cè)柱 時(shí)間: 2025-3-26 15:07
Hermann Lang,Stefan Schilling,Hermann Faller a local and parenchimal inflammatory reaction characterised by astroglia and microglia activation has been reported in several brain pathologies including prion diseases and various dementias like Alzheimer’s disease and the AIDS dementia complex. In agreement, stimulation of the calcium-dependent 作者: atrophy 時(shí)間: 2025-3-26 20:39 作者: 幸福愉悅感 時(shí)間: 2025-3-26 21:58
https://doi.org/10.1007/978-3-642-91836-0ential application of mGlu5 receptor antagonists in chronic neurodegenerative disorders, such as Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s disease (AD). MGlu2/3 receptor agonists inhibit glutamate release, and also promote the synthesis and release of neurotrophic factors in astrocytes. Th作者: Outmoded 時(shí)間: 2025-3-27 04:25
https://doi.org/10.1007/978-3-663-02455-2 such as caspase-3. Essentially all subcellular compartments, including the endoplasmic reticulum, mitochondria and nucleus are involved in the excitotoxic process. Excitotoxic cascades are initiated in postsynaptic dendrites where glutamate receptors are most highly concentrated, and may either cau作者: 挖掘 時(shí)間: 2025-3-27 09:20
https://doi.org/10.1007/978-3-662-32989-4hat SE-induced excitotoxic injury is not required for the development of long-term disrupt ion of neuronal function in the aftermath of SE. In contrast to SE, recurrent intermittent brief seizures such as those typically associated with epilepsy, do not necessar ily cause neuronal inj ury. In patien作者: congenial 時(shí)間: 2025-3-27 11:30 作者: arthroplasty 時(shí)間: 2025-3-27 14:24
Erfahrungen mit neuen Bauweisen,ructural impairment observed following experimental TBI after administration of compounds designed to attenuate glutamate excitotoxicity raised high expectations for improvement of outcome following clinical TBI, and we summarize the phase III clinical trials conducted thus far with glutamate recept作者: CRUMB 時(shí)間: 2025-3-27 18:42
https://doi.org/10.1007/978-3-322-96441-0nuclein and parkin. Moreover, compelling evidence supports the involvement of mitochondrial metabolism failure as an essential cofactor in the pathogenesis of PD. Interestingly, some environmental toxins are thought to be able to act as mitochondrial toxins. The comprehension of the pathways leading作者: Scintigraphy 時(shí)間: 2025-3-28 00:49
,Führerscheingutachten bei Schizophrenen,o the motor and cognitive deficits, which occur in HD. The development of transgenic mouse models has furthered the evidence that excitotoxicity plays a role in HD pathogenesis. Although mice with short fragments of huntingtin show resistance to excitotoxic lesions, transgenic mice with full-length 作者: innate 時(shí)間: 2025-3-28 04:39
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), 作者: Diskectomy 時(shí)間: 2025-3-28 09:46
or AMPA receptor trafficking in long-term potentiation (LTP) and in long-term depression (LTD). Here we focus on the mechanisms that underlie the modulation of AMPA receptors during the synaptic plasticity.作者: MULTI 時(shí)間: 2025-3-28 12:44 作者: 使入迷 時(shí)間: 2025-3-28 15:28
Reaktionen einer Art Ausgangsmolekeln cell culture studies. Since oligodendrocyte damage by glutamate excitotoxicity has been described in a number of unrelated white matter conditions, glutamate excitotoxicity may be a common pathway in white matter injury.作者: 紡織品 時(shí)間: 2025-3-28 22:28 作者: GLIB 時(shí)間: 2025-3-29 01:56
Glutamate Excitotoxicity in Multiple Sclerosis cell culture studies. Since oligodendrocyte damage by glutamate excitotoxicity has been described in a number of unrelated white matter conditions, glutamate excitotoxicity may be a common pathway in white matter injury.作者: Sciatica 時(shí)間: 2025-3-29 07:09
https://doi.org/10.1007/978-3-642-91570-3inking calcium influx to delayed cell death caused by excitatory amino acids (Choi, 1987). More work has linked activation of excitatory amino acid receptors to free radical generation and nitric oxide, both of which may lead to oxidative stress (Dawson et al., 1991: Lafon-Cazal et al., 1993).作者: Jocose 時(shí)間: 2025-3-29 10:50
https://doi.org/10.1007/978-3-662-32987-0animal models of amyotrophic lateral sclerosis. Results from ongoing and future clinical trials will give definitive answer to the relevance of AMPA-mediated excitotox icity in patients with amyotrophic lateral sclerosis.作者: 割公牛膨脹 時(shí)間: 2025-3-29 13:22 作者: Bph773 時(shí)間: 2025-3-29 18:08 作者: 侵略者 時(shí)間: 2025-3-29 20:49 作者: 浪費(fèi)時(shí)間 時(shí)間: 2025-3-30 02:56 作者: pus840 時(shí)間: 2025-3-30 07:01 作者: FLASK 時(shí)間: 2025-3-30 11:40
AMPA Receptor and Synaptic Plasticityor AMPA receptor trafficking in long-term potentiation (LTP) and in long-term depression (LTD). Here we focus on the mechanisms that underlie the modulation of AMPA receptors during the synaptic plasticity.作者: Ordnance 時(shí)間: 2025-3-30 12:35
H. Zebe,H. C. Mehmel,D. Opherk,W. M?urerhe abnormal prion protein. Clearly, an understanding of the mechanisms by which prion mediated neuronal death occurs might lead to treatments that would prevent the life threatening nature of these diseases.作者: 環(huán)形 時(shí)間: 2025-3-30 17:46
https://doi.org/10.1007/978-3-642-86743-9 stress-associated protein kinases, caspases, and transcription factors, and production of cytotoxic free radicals. The chapter on HIV-1 associated dementia will review recently identified pathways to neuronal injury and death triggered by the virus or parts of it, and potential approaches to development of applicable therapeutic intervention.作者: Abduct 時(shí)間: 2025-3-30 21:04
Neurotoxicity and Prion Diseasehe abnormal prion protein. Clearly, an understanding of the mechanisms by which prion mediated neuronal death occurs might lead to treatments that would prevent the life threatening nature of these diseases.作者: Hyperopia 時(shí)間: 2025-3-31 03:21 作者: Orgasm 時(shí)間: 2025-3-31 08:21 作者: synovitis 時(shí)間: 2025-3-31 09:41 作者: Ingredient 時(shí)間: 2025-3-31 16:02 作者: 巫婆 時(shí)間: 2025-3-31 18:33 作者: dagger 時(shí)間: 2025-3-31 23:25
Hermann Lang,Stefan Schilling,Hermann Fallerreceptors 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
