[NFS-03-4] TDP-43によるインスリン分泌制御
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.
Dr. Masahisa Katsuno received his M.D. in 1995 and his Ph.D. in Neurology in 2003, both from Nagoya University in Nagoya, Japan. Following an postdoctoral fellowship at Japan Foundation for Aging and Health, he became an associate professor of Institute of Advanced research, Nagoya University, at 2006, and then an associate professor of Department of Neurology, Nagoya University, at 2012. From July 2015, he has been a professor of Department of Neurology, Nagoya University. He also serves as a Vice Dean and the coordinator of the Doctoral Program for World-leading Innovative & Smart Education (WISE) in Nagoya University Graduate School of Medicine.
抄録パスワード認証
パスワードは抄録集に記載してあります。