第50回日本神経学会総会
＜シンポジウム2―1＞ALS治療法開発の将来孤発性ALS疾患モデルによる病態解明と治療法開発
田中 章景1）, 和座 雅浩1）, 山本 正彦2）, 祖父江 元1）
1）名古屋大学大学院医学系研究科・神経内科学〔〒466-8550 名古屋市昭和区鶴舞町65〕
2）愛知学院大学心身科学部・健康科学科
The mechanisms underlying motor neuron degeneration in amyotrophic lateral sclerosis (ALS) remain poorly understood even now 140 years after the first description of the disease in 1869 by Jean-Martin Charcot. Exploration of pathogenesis of ALS has long been dependent on transgenic animal models with mutations in the copper/zinc superoxide dismutase 1 (SOD1) gene. However, the lack of therapeutic concordance between these animal models and human sporadic ALS patients is troubling. The reasons include that there might exist the differences of pathogenesis between sporadic and familial ALS and/or the disease models for sporadic ALS have not bee established. We have been working on screening motor neuron-specific genes critical for pathogenesis of sporadic ALS using cDNA microarray and laser capture microdissection techniques. Many of the resultant genes are of intense interest and may provide a powerful tool for determining the molecular mechanisms of sporadic ALS. In particular, dynactin-1, a major component of dynein/dynactin complex and several cell cycle-related genes are the targets of our research. Development and analysis of new disease models for sporadic ALS based on these genes will open an avenue for novel therapeutics.
Full Text of this Article in Japanese PDF (408K)
(臨床神経, 49：811−813, 2009)
key words：孤発性筋萎縮性側索硬化症, 遺伝子発現解析, 疾患モデル, ダイナクチン1
（受付日：2009年5月21日）
