第60回日本神経学会学術大会

セッション情報

シンポジウム

[S-02] Genetic and neuropathological approach decipher the molecular mechanism of idiopathic central nervous system demyelinating diseases

2019年5月22日(水) 09:50 〜 11:50 第9会場 (大阪国際会議場12F 特別会議場)

座長:磯部 紀子(九州大学大学院医学研究院脳神経治療学), 眞﨑 勝久(九州大学大学院医学研究院神経内科学分野)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.

Philip L. De Jager (Center for Translational & Computational Neuroimmunology and Multiple Sclerosis Center, Department of Neurology, Columbia University Medical Center)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.

松下 拓也1, 磯部 紀子3, 佐藤 眞也2, 山本 健4, 渡邉 充2, 中村 優理2, 吉良 潤一2, 日本多発性硬化症遺伝子コンソーシアム2 (1.九州大学病院神経内科, 2.九州大学大学院医学研究院神経内科学, 3.九州大学大学院医学研究院脳神経治療学, 4.久留米大学医学部医学科医化学講座)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.

Qiu Wei (The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, China)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.

林 史恵1, 磯部 紀子2, Jacob Glanville3, 中村 優理2, 松下 拓也1, 吉良 潤一1 (1.九州大学医学研究院脳神経内科学, 2.九州大学医学研究院脳神経治療学, 3.Computational and Systems Immunology Program, Stanford University School of Medicine)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.

眞崎 勝久 (九州大学病院 神経内科)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.