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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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

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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

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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

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Precursor

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

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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

Manifest

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

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