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Article type: Research Article
Authors: Ludolph, Albert C. | Meyer, Thomas | Riepe, Matthias W. | Volkel, Helge
Affiliations: Department of Neurology, University of Ulm, D-89075 Ulm, Steinhövelstraße 9, Germany
Note: [] Corresponding author: Albert C. Ludolph, Department of Neurology, University of Ulm, D-89075 Ulm, Steinhövelstraße 9, Germany. Tel.: +49 731 5027970; Fax: + 49 731 5027979; E-mail: [email protected]
Abstract: Amyotrophic lateral sclerosis is a progressive fatal disorder devastating the spinal cord and brain in humans. Excitotoxicity has been suggested to be involved in the pathogenesis of amyotrophic lateral sclerosis. This hypothesis has driven a wealth of basic research and stimulated development of neuroprotective therapies for chronic neurodegenerative disorders. As a result of these efforts, riluzole, an antiglutamatergic drug, has been established in the therapy of amyotrophic lateral sclerosis. A transgenic mouse showing features of amyotrophic lateral sclerosis has been subsequently engineered enabling studies of the disease in vivo. However, despite considerable progress, the etiology of amyotrophic lateral sclerosis remains obscure and the disturbances in excitatory neurotransmission should by no means be regarded as exclusive to the pathogenesis of the disease.
Keywords: amyotrophic lateral sclerosis, Cu/Zn SOD, EAAT2, excitotoxicity, neurolathyrism, riluzole
Journal: Restorative Neurology and Neuroscience, vol. 13, no. 1-2, pp. 59-67, 1998
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