Sat. Oct 12, 2019 2:50 PM - 4:30 PM Room 15 (Palace Room B)

Organizer / Chair: ‌Brian DEAN (Florey Institute for Neuroscience and Mental Health / Centre for Mental Health, Swinburne University, Australia), Co-chair: Takeo YOSHIKAWA (RIKEN Center for Brain Science, Japan), Discussant: ‌Akinori NISHI (Department of Pharmacology, Kurume University School of Medicine, Japan)

Psychiatric disorders are complex and occur in individuals with a genetic predisposition following an encounter with deleterious environmental factors. The interaction between environment and the genome occurs through epigenetic mechanisms and the outcome is to cause changes in gene expression. This knowledge underpins the ongoing use of human postmortem CNS to understand the pathophysiologies of psychiatric disorders by identifying the changes in molecular cytoarchitecture brought about by changed gene expression. In Japan efforts are being made to create a Network of Brain Banks that will include tissue from subjects with psychiatric disorders. However, there is already collaborations between Japanese scientists and the Melbourne Psychiatric Brain Bank that are shedding light on the pathophysiology of psychiatric disorders. The objective of this symposium is to update delegates on outcomes from the study of brain tissue from the brain bank and how they are advancing knowledge on the molecular pathology of psychiatric disorders. The first speaker, Brian Dean, will provide a brief description of the Melbourne Psychiatric Brain Bank and will then review how recent studies of the cortical human transcriptome using tissue from the Brain Bank are providing new information on the underlying pathophysiologies of schizophrenia, major depressive disorders and bipolar disorders. Whilst such transcriptomics data are increasing knowledge of the potential causes of psychiatric disorders, the challenge remains as to how such “omics” data can be interpreted. Hence, the second presenter, Hirotaka Sekiguchi, will present new data on changes in levels of the cortical and sub-cortical dopamine transporter in schizophrenia and mood disorders. These data will be used to suggest mechanisms by which changes in dopamine homeostasis is involved in the pathophysiologies of schizophrenia and major depressive disorders. The final two speakers in the Symposium will focus on changes in lipid metabolism in the corpus callosum from subjects with schizophrenia. Neuroimaging studies have suggested changes in the corpus callosum are particularly prevalent in schizophrenia. The corpus callosum is the bridge between the brain hemispheres containing wide thick nerve tracks. Hence, changes in the functioning of lipids such as phospholipids and sphingolipids in this CNS region would have profound effects on CNS function. Hence, the third speaker, Chie Shimamoto-Mitsuyama, will review evidence that suggests changed lipid metabolism may be present in the corpus callosum from subjects with schizophrenia. The Symposium will close with the forth speaker, Kayoko Esaki, who will argue there is changes in the regulation of sphingolipid-signaling pathway in the corpus callosum from schizophrenia. In conclusion, this symposium will provide an update to the delegates at AsCNP on new findings, predominantly by young Japanese scientists, on the molecular pathophysiologies of schizophrenia and mood disorders.