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Plenary Lectures

HT Chang Memorial Lecture

Speaker:
Graham Leon Collingridge
University of Toronto/Mount Sinai Hospital, Canada
Time:
08:30-09:15 Oct. 13
Title:

Dr. Graham L. Collingridge is a British neuroscientis and professor at the University of Toronto and at the University of Bristol. He is also a senior investigator at the Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital in Toronto. Professor Collingridge's research focuses on the mechanisms of synaptic plasticity in health and disease, in particular, understanding synaptic plasticity in molecular terms and how pathological alterations in these processes may lead to major brain disorders, such as Alzheimer's disease. Professor Collingridge was with Professors Tim Bliss and Richard Morris as the first UK scientists to share the Brain Prize, one of the world's most coveted science prizes.

CP Wu Memorial Lecture

Speaker:
Abdel El Manira
Karolinska Institute, Sweden
Time:
08:30-09:15 Oct. 12
Title:
Brain circuits for motor actions

Dr. Abdel El Manira is a Distinguished Professor in Neuroscience at the Karolinska Institute. His laboratory has long been making fundamental contributions to the understanding of the neural control of locomotion. His studies in this area are transforming our view of spinal motor-control systems and setting a new agenda for future research in this area. Professor El Manira is an elected member of the Royal Swedish Academy of Sciences, the Royal Academy of Sciences and Technologies of Morocco, and the Academy of Europe. He is also a member of the Nobel Assembly at the Karolinska Institute.

TCCI Lecture

Speaker:
Trevor W.Robbins
University of Cambridge
Time:
08:30-09:15 Oct. 11
Title:
Neurobehavioural basis of compulsion in OCD and drug addiction

Trevor Robbins was appointed in 1997 as the Professor of Cognitive Neuroscience at the University of Cambridge. He was formerly Professor of Experimental Psychology (and Head of Department) at Cambridge from October 2002-October 2017. He is also Director of the Behavioural and Clinical Neuroscience Institute (BCNI), jointly funded by the Medical Research Council and the Welcome Trust. The mission of the BCNI is to inter-relate basic and clinical research in psychiatry and neurology for such conditions as Parkinson's, Huntington's, and Alzheimer's diseases, frontal lobe injury, schizophrenia, depression, drug addiction and developmental syndromes such as attention deficit/hyperactivity disorder. Trevor's current research is focused on impulsive-compulsive disorders (such as OCD and drug addiction) and fronto-striatal systems of the brain. In 2018 he became an Honorary Professor at Fudan University, Shanghai.

Plenary Lectures

Speaker:
Haruhiko Bito
University of Tokyo Graduate School of Medicine, Japan
Time:
13:30-14:15 Oct. 13
Title:
Multiplex imaging of neural activity and signaling dynamics

Professor Haruhiko Bito received postdoctoral training at Richard Tsien Laboratory, his main contribution was to analyze the phosphorylation modification of specific proteins in neurons after activation and its relationship with gene expression. Its research direction in the laboratory of Tokyo University is to analyze the mechanism of neuronal signal transduction behind the complex biological processes of the brain, including the identification and mechanism analysis of important mediators, and to develop new techniques for more detailed control and tracking of neuronal activity and the dynamic changes of signal molecules.

Speaker:
Junying Yuan
Department of Cell Biology, Harvard Medical School
Time:
Title:
The role of RIPK1 in mediating neuroinflammation

Junying Yuan made critical contributions to our understanding of apoptosis and necroptosis, two fundamental mechanisms that regulate the survival and death of mammalian cells. Her Ph.D. work, as a student at the Harvard Medical School and conducted in the laboratory of H. Robert Horvitz at the Massachusetts Institute of Technology, provided the first insight into the mechanism of programmed cell death in the nematode C. elegans. Yuan started her own lab in 1990 at the Cardiovascular Research Center, Massachusetts General Hospital, to test her hypothesis that a similar programmed cell death mechanism might exist in mammalian cells. Her daring hypothesis was proved two years later when her laboratory demonstrated that the mammalian interleukin-1b converting enzyme (later named caspase-1) is a functional homologue of C. elegans cell death gene product Ced-3 (Miura et al. 1993) and inhibition of caspase activation blocks neuronal cell death induced by trophic factor deprivation (Gagliardini et al. 1994). These works provided the first insight into the molecular mechanism that regulates apoptosis in mammalian cells. Subsequently, after her move in 1996 to Department of Cell Biology, Harvard Medical School, Yuan lab discovered necroptosis, a regulated necrotic cell death mechanism, and the role of RIPK1 kinase as a key mediator of necroptosis (Degterev et al. 2005, Degterev et al. 2008). This discovery overturned the traditional dogma that necrosis can only be a form of unregulated passive cell death and demonstrated the possibility of inhibiting necrotic cell death in multiple forms of degenerative and inflammatory human diseases. A small molecule inhibitor of RIPK1 kinase (Nec-1) discovered by Yuan lab is currently in preparation for a human clinical trial targeting neurodegenerative disease.

Speaker:
Ronald Stanton Duman
Yale University Sochool of Medicine
Time:
Title:
Neurobiology of Stress, Depression and Antidepressants: Remodeling Synaptic Connections

Studies in Dr. Duman's laboratory are focused on identifying the molecular and cellular adaptations that underlie the actions of antidepressant drugs and stress. This includes adaptations of receptors, signal transduction proteins, gene transcription factors, neurotrophic factors, and regulation of synaptic processes and even birth of new neurons (neurogenesis) in the adult brain. Preclinical and clinical studies support the hypothesis that neuronal atrophy and cell loss in response to stress contribute to mood disorders. Conversely, the therapeutic action of antidepressants may occur in part via blocking or reversing these damaging effects of stress. A variety of molecular approaches combined with cellular and behavioral studies are conducted to elucidate the basis of complex behavioral abnormalities.

 

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