Conjoint Principle Research Scientist, NeuRA
+612 9399 1626
My research is broadly focused on determining modifiable risk factors for the development of psychosis and mood disorders, using a combination of techniques from cognitive psychology, neuroscience, genetics, and more recently epidemiology. Major funded research themes include ‘imaging genetics’ investigations of psychotic and mood disorders, and population-level research to determine the interaction of biological and environmental risk factors for psychotic disorders over the life course. My early research focused on cognitive and emotion regulation disturbances in a variety of psychiatric disorders and high risk populations, and was translated into social cognitive remediation tools used increasingly in standard psychiatric care. I am now focusing my efforts on large, well characterised clinical and population samples where possible, to faciliate the integrated study of social and biological determininants of psychosis and related conditions. I am particularly interested in stress-related biological changes that may operate differently in response to stressors experienced at different developmental stages. These projects are conducted in close collaboration with NSW government partners and colleagues at Neuroscience Research Australia (NeuRA), the Black Dog Institute, and the UNSW School of Psychology, with other national collaborators at the University of Newcastle, Monash University, the University of Melbourne, and Macquarie University. I also collaborate with researchers at the University of Leiden (The Netherlands), and the Ludwig-Maximilians-University of Munich (Germany).
LEAH GIRSHKIN PhD Student
STACY TZOUMAKIS Lecturer
NINA TEROGANOVA PhD Student
Postdoctoral Research Fellow, UNSW School of Psychiatry
: 02 9399 1866
DR KRISTIN LAURENS Senior Research Scientist
JESSECA ROWLAND PhD Student
KIMBERLIE DEAN Principle Research Scientist
FELICITY HARRIS Research Officer
PROF VAUGHAN CARR Senior Principle Research Scientist
Contrary to some – but not all – previous findings, this study of a large sample of schizophrenia cases and healthy controls reveals no evidence for association between grey matter alterations and variation in rs1344706 (ZNF804A). Differences in sample sizes and ethnicities may account for discrepant findings between the present and previous studies.
Trauma-related increases in activation of the left IFG were not associated with performance differences, or dependent on clinical diagnostic status; increased IFG functionality may represent a compensatory (overactivation) mechanism required to exert adequate inhibitory control of the motor response.