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

幸福愉悦感

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

Outmoded

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

挖掘

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

congenial

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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

CRUMB

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

Scintigraphy

,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

innate

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),

Diskectomy

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.

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