Date: 2 July 2024 (Tuesday) Time: 11:00am - 12:30pm
Format:Virtual (Zoom)
Hosted by: Adrian TEO, IMCB, Singapore
Speakers' information
Kazunobu SAWAMOTO Nagoya City University Graduate School of Medical Sciences, Japan
"Building bridges in the brain: Promoting neuronal migration for recovery"
ABSTRACT In many animal species, neural stem cells persistently generate new neurons along the brain ventricular wall throughout life. Following brain injuries, these newly generated neurons exhibit migratory behavior towards the affected regions, where they undergo maturation. Within the injured brain, this migration is facilitated by endogenous scaffolds, such as blood vessels and radial glial fibers. Utilizing artificial scaffolds or pharmacological agents to augment neuronal migration has shown promise in promoting neuronal regeneration and subsequent functional recovery. In this presentation, I will introduce our recent research findings and propose innovative therapeutic modalities aimed at leveraging endogenous neurogenesis for repairing the injured brain.
BIO Kazunobu Sawamoto is Professor of Developmental and Regenerative Neurobiology at Nagoya City University Graduate School of Medical Sciences. He received his Ph.D. in 1996 under the supervision of Prof. Katsuhiko Mikoshiba from The University of Tokyo for his work on Drosophila neural development. He then worked as a Research Associate in Prof. Hideyuki Okano's laboratory at University of Tsukuba (1996-1997) and Osaka University (1997-2003). In 2001-2003, he also worked as a visiting postdoc in Prof. Arturo Alvarez-Buylla's laboratory at University of California San Francisco. He was appointed Assistant Professor at Keio University in 2003, Associate Professor at Keio University in 2005, Professor at Nagoya City University in 2007, Adjunct Professor at National Institute for Physiological Sciences in 2016, and Director of Institute of Brain Science, Nagoya City University in 2021. His work focuses on the mechanisms for neurogenesis and neuronal migration in the postnatal brain.
LI ZENG National Neuroscience Institute, Singapore
"Modelling neurological diseases to pinpoint the cause of neurodegeneration"
ABSTRACT Recent advance in stem cell and brain organoid technologies provides advancements allowing us to delve into the specific cellular pathology of neurological disorders within a human context. We have developed human cerebral organoids derived from PBMCs obtained from dementia patients who carry diverse genetic mutations linked to cognitive impairments. These mutations include PS1, NOTCH3, and CSF1R. We utilized a combination of scRNA sequencing, bioinformatic analysis, and functional cellular assays to explore the impact of various genetic mutations associated with neurological disorders on different cell types within the brain, such as neurons, astrocytes, microglia, and endothelial cells. In this talk, I will present our recent findings on the dysfunction of various cellular processes across different cell types and highlight the complex nature of disease origins, pointing toward a multifaceted etiology.
BIO Li ZENG is an Associate Professor and Principal Investigator at the National Neuroscience Institute (NNI), Singapore. She earned her BSc in Biology from Beijing Normal University and completed her Ph.D. in Biochemistry at the University of Glasgow. Subsequently, she undertook postdoctoral training in the Signal Transduction group at the Institute of Molecular and Cell Biology (IMCB), National University of Singapore (NUS), before joining the Developmental Biology group at IMCB, A*STAR as a Research Scientist. During this tenure, she investigated TAG1-APP signaling in regulating neurogenesis and its relevance to Alzheimer’s disease. Since 2009, Dr. Zeng has led her research team at NNI. Collaborating closely with NNI clinicians and clinician scientists, her research focuses on using the pre-clinical mouse model, and 2D iPSCs and 3D brain organoid-derived from neurological diseases patients to pinpoint the cause of neurodegeneration and identify novel therapeutic interventions.