Associate Professor Tomoko Soga is the Head of Drug Discovery Capability, including the iPS cell facility, at the Brain Research Institute Monash Sunway (BRIMS). She joined Monash University in 2006 from the National Institute of Neuroscience, National Center of Neurology and Psychiatry, Japan. She obtained her BSc and MSc from Kyoto Institute of Technology. Upon obtaining her PhD from Nippon Medical School, she was a postdoctoral fellow at The Rockefeller University in New York, USA. Her research focus has been on the neuronal mechanisms of depression, in particular brain serotonergic pathways in social stress-induced depression. She has published over 50 papers with high ISI citations which have appeared in internationally renowned journals such as Endocrinology, Neuropharmacology, PNAS. She has received several awards such as Narishige award for neuroscience and from the Japan foundation for aging and health. She also serves as an associate and guest editor of several journals, such as 'Frontiers in Aging Neuroscience', 'Frontiers in Endocrinology', and 'Frontiers in Neuroscience'. She is a council member of the Asia and Oceania Society for the Comparative Endocrinology.

Mental disorders such as depression and anxiety are closely associated with social stress in humans, in addition to their biological background. Social stress activates the hypothalamic–pituitary–adrenal axis and increases the risk of developing mental disorders. In fact, social stress such as social isolation or social defeat stress deregulates the neuroendocrine system, neurotransmitters and the reproductive pathways. The goal of our research team is to elucidate the causes of social stress induced depression to develop fundamental therapies and early diagnostic methods. To identify genetic susceptibility for depression and social stress associated environmental factors will lead to better understanding of neurobiological mechanisms of depression. Currently, animal models have been developed that use social isolation or social defeat stress to induce neuronal dysfunctions and behaviour changes that might be similar to those occurring in the course of the development of depression. In recent years, we try to use clinical samples including cellular models (human iPS cells) using advanced technologies of genomics.