Molecular mechanism and therapeutics of amyotrophic lateral sclerosis : proceedings of the International Symposium on Molecular Mechanism and Therapeutics of Amyotrophic Lateral Sclerosis, Japan, 22-24 September 2000

著者

    • International Symposium on Molecular Mechanism and Therapeutics of Amyotrophic Lateral Sclerosis
    • Abe, Koji

書誌事項

Molecular mechanism and therapeutics of amyotrophic lateral sclerosis : proceedings of the International Symposium on Molecular Mechanism and Therapeutics of Amyotrophic Lateral Sclerosis, Japan, 22-24 September 2000

editor, Koji Abe

(International congress series, no. 1221)

Elsevier, 2001

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注記

Includes bibliographical references and index

"Neurology" --Cover

内容説明・目次

内容説明

This volume covers the latest findings on the molecular mechanism and therapeutics of amyotrophic lateral sclerosis (ALS), including important research on 1) pathological characteristics and epidemiology of ALS, 2) selective vulnerability of spinal motor neurons, 3) genetic abnormality of ALS and neurotrophin, 4) mechanism of motor neuron death and glutamate toxicity, 5) motor axon, axonal transport, neurofilament, and glycation, 6) basic therapeutic approach, and 7) clinical therapeutic approach. The surprising discovery of Cu/Zn superoxide dismutase (SOD1) gene mutations in a part of familial ALS in 1993 has had a strong impact on all neuroscientists and clinicians dealing with this disease. This volume aims to help them to progress their future basic and clinical investigations, and to enhance strong scientific collaboration in elucidating the molecular mechanism and discovering the essential therapeutics of the disease.

目次

Preface. Pathological characteristics and an epidemiology of ALS. Pyramidal tract pathology in amyotrophic lateral sclerosis---axon staining reveals degeneration undisclosed on myelin staining (I. Nakano). Molecular pathology of anal spheroid in ACS (T. Kate). Basophilic cytoplasmic inclusions in amyotrophic lateral sclerosis (K. Okamoto et al.). Expression of cathepsins in the motor neurons of amyotrophic lateral sclerosis (H. Kikuchi et al.). Epidemiology of motor neuron disease in Miyakonojo basin, Kyushu, Japan (R. Okubo et al.). Intracytoplasmic inclusions with overexpressed mutant SOD1 gene (R. Nakano, T. Koide, S. Tsuji). Selective vulnerability of spinal motor neurons. Induction of cell cycle dependent proteins in spinal motor neurons (M. Sakurai et al.). Apoptosis of spinal motor neuron after ischemia (T. Hayashi et al.). Motor neuron apoptosis by glutamate (Y. Manabe et al.). Subcellular localization of Cu,Zn-SOD and its role in the pathogenesis of FALS (Y. Kira et al.). Zinc-deficient superoxide dismutase: A possible mechanism for ALS (A.G. Estevez). ROS/RNS/dicarbonyl stress to spinal motor neurons in vitro (K. Shinpo et al.). An experimental model of Kii-ALS. A chronic low-CaMg high-Al diet induces neuronal loss and skin changes (T. Kihira et al.). Establishment of local cooling model against transient spinal cord ischemia (N. Motoyoshi, M. Sakurai, K. Tabayashi). Genetic abnormality of ALS and neurotrophin. SOD1 mutation and clinical features of familial amyotrophic lateral sclerosis (K. Abe et al.). A two-base deletion of SOD1 gene in a Japanese FALS family (Y. Watanabe et al.). A family with a novel SOD1 gene mutation (T. Murakami et al.). Familial ALS with a novel homozygous mutation of Cu/Zn SOD gene (M. Kato et al.). CAG/CTG repeat expansions are not commonly involved in the pathogenesis of amyotrophic lateral sclerosis (M. Morita et al.). Association study in a-synuclein polymorphism in spor

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