60th Annual Meeting of the Japanese Society of Neurology

Session information

Symposium

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

Wed. May 22, 2019 9:50 AM - 11:50 AM Room 9 (Osaka International Convention Center 12F Conference Hall)

Chair:Noriko Isobe(Department of Neurological Therapeutics, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Japan), Katsuhisa Masaki(Department of Neurology, Graduate School of Medical Science, Kyushu University, Japan)

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, USA)

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.

Takuya Matsushita1, Noriko Isobe3, Shinya Sato2, Ken Yamamoto4, Mitsuru Watanabe2, Yuri Nakamura2, Jun-ichi Kira2, Japan Multiple Sclerosis Genetics Consortium2 (1.Department of Neurology, Kyushu University Hospital, Japan, 2.Department of Neurology, Graduate School of Medical Sciences, Kyushu University, 3.Department of Neurological Therapeutics, Graduate School of Medical Sciences, Kyushu University, 4.Department of Medical Chemistry, School of Medicine, Kurume University)

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.

Fumie Hayashi1, Noriko Isobe2, Jacob Glanville3, Yuri Nakamura2, Takuya Matsushita1, Jun-ichi Kira1 (1.Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Japan, 2.Department of Neurological Therapeutics, Graduate School of Medical Sciences, Kyushu University, 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.

Katsuhisa Masaki (Department of Neurology, Graduate School of Medical Science, Kyushu University, Japan)

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.