[NFS-03-1] ALSの病原蛋白質に対する抗体治療戦略
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting from loss of upper and lower motor neurons. Although the majority of ALS cases are sporadic, 5–10% of patients have a positive family history. The pivotal histopathological finding of sporadic ALS is intraneuronal aggregates of TDP-43. Recent advancement in genetics identified a variety genetic cause of ALS, including C9orf72, TDP-43, FUS and SOD1. This provides a tight link between this disease and frontotemporal lobar degeneration (FTLD) as well as important molecular insight into ALS/FTLD such as dysregulated RNA metabolism, disrupted protein quality control, axonal transport impairment and nuclear transport deficit, among others. In this symposium, cutting-edge research on the pathogenesis and therapy development for ALS and related disorders will be discussed.
Education, Professional Training and Employment:
1985-1991 Student, Faculty of Medicine, Kyoto University
1991-1992 Resident, Dept. of Neurology, Kyoto University Hospital
1992-1996 Staff Doctor, Dept. of Neurology, Sumitomo Hospital
1996-2000 Ph.D. Student. Department of Neurology, Kyoto University Graduate School of Medicine
2000-2003 Staff Scientist. Brain Science Institute, RIKEN
2003-2006 Postdoctoral fellow of Laval University. Quebec City, CANADA
2006-2009 Assistant Professor, Shiga University of Medical Science (SUMS)
2009-2013 Associate Professor and Principal Investigator, SUMS
2013-2016 Associate Professor and Laboratory Head, Department of Neurology
Kyoto University Graduate School of Medicine
2016-present Professor and Chair, Department of Neurology, SUMS
Awards:
Fellowship of Canadian Institute of Health and Research (CIHR) (2005-2006)
Brain Star Award (2006); CIHR
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