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• Vol.47から1まではこちら
  会員専用

• ホーム
• 47巻11号
• 臨床神経, 47：934−937, 2007
• 47巻11号目次

第48回日本神経学会総会

＜シンポジウム9-2＞神経変性疾患の動物モデル
筋萎縮性側索硬化症

山中　宏二

理化学研究所脳科学総合研究センター山中研究ユニット〔〒351-0198　埼玉県和光市広沢2-1〕

Dominant mutation in the gene of superoxide dismutase 1 (SOD1) leads amyotrophic lateral sclerosis (ALS), an adult-onset progressive fatal motor neuron disease. Recent research progress in ALS has been made by the use of transgenic mouse model of familial ALS, which expresses mutant form of SOD1 and recapitulates the phenotype and pathology of motor neuron disease. There is accumulating evidence indicating non-cell-autonomous motor neuron death in ALS mouse model. In this symposium, I review the recent advance of ALS research focusing on the development of animal models, the role of glial cells in ALS, and therapeutic intervention of rodent models and discuss their prospect.

(臨床神経, 47：934−937, 2007)
key words：ALS, SOD1, トランスジェニックマウス, 非自律性神経細胞死, ミクログリア

（受付日：2007年5月16日）