[NFS-03-3] Glia-immune communication in ALS
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
1992, MD Kyoto University
2000, Ph.D. Graduate School of Medicine, Kyoto University
Positions and Employment
1992-1996 Medical Residency (Kyoto University Hospital and others)
2001-2006 Postdoctoral Fellow, University of California, San Diego
2006-2009 Unit Leader, RIKEN Brain Science Institute
2009-2013 Laboratory Head, RIKEN Brain Science Institute, Japan
2013-current Professor, Research Institute of Environmental Medicine (RiEM), Nagoya University
2016-2020 Director, RiEM, Nagoya University
Other Experience and Professional Memberships
Director, Treasurer, The Japan Neuroscience Society
Councilor, Japanese Society of Neurology, Japanese Society of Neuroimmunology, Japanese Society of Neurochemistry
Associate Editor: Science Advances, FEBS Open Bio, Clin Exp Neuroimmunology, Section Editor: Neuroscience Research, Editorial Board: Molecular Brain
Honors
2004 Carrier Developmental Award, Muscular Dystrophy Association, USA
2013 Year 2013 Award, Japanese Society of Neurology
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