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
The objective of the current study was to quantify the degree of white matter (WM) abnormalities in chronic and virally suppressed HIV-infected (HIV+) persons while carefully taking into account demographic and disease factors. Diffusion tensor imaging (DTI) was conducted in 40 HIV- and 82 HIV+ men with comparable demographics and life style factors. The HIV+ sample was clinically stable with successful viral control. Diffusion was measured across 32 non-colinear directions with a b-value of 1000 s/mm; fractional anisotropy (FA) and mean diffusivity (MD) maps were quantified with Itrack IDL. Using the ENIGMA DTI protocol, FA and MD values were extracted for each participant and in 11 skeleton regions of interest (SROI) from standard labels in the JHU ICBM-81 atlas covering major striato-frontal and parietal tracks. We found no major differences in FA and MD values across the 11 SROI between study groups. Within the HIV+ sample, we found that a higher CNS penetrating antiretroviral treatment, higher current CD4+ T cell count, and immune recovery from the nadir CD4+ T cell count were associated with increased FA and decreased MD (p < 0.05-0.006), while HIV duration, symptomatic, and asymptomatic cognitive impairment were associated with decreased FA and increased MD (p < 0.01-0.004). Stability of HIV treatment and antiretroviral CNS penetration efficiency in addition to current and historical immune recovery were related to higher FA and lower MD (p = 0.04-p < 0.01). In conclusion, WM DTI measures are near normal except for patients with neurocognitive impairment and longer HIV disease duration.
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.