NSW Chair of Schizophrenia Research, based at NeuRA and UNSW
Professor, School of Psychiatry, UNSW
Professor, Department of Neuroscience and Physiology, Upstate Medical University, New York
+612 9399 1717
Cyndi’s research is focused on the molecular developmental neurobiology of schizophrenia. She earned a PhD in Biomedical Science at Mount Sinai School of Medicine, New York City and completed postdoctoral training at the National Institute of Mental Health rising to the level of Unit Chief of Molecules in the Neurobiology and Development of Schizophrenia Unit. Her awards include the Eli Lilly Young Investigator Award, NIH Fellows Award for Research Excellence, Independent Investigator Award and two Young Investigator Awards from NARSD. She has lectured throughout the world and contributed to over 150 publications.
Dr Purves-Tyson is an Associate Investigator in a cross-discipline collaboration between researchers from multiple facilities in a pilot study investigating the microbial diversity of people experiencing schizophrenia both in the early stages of illness and in established illness, in relation to metabolic parameters, inflammation and intervention with diet and exercise.
The pathophysiology of dopamine dysregulation in schizophrenia involves alterations at the level of the level. Given that inflammatory mediators such as cytokines can influence the functional properties of midbrain dopamine neurons, midbrain inflammation may play a role in schizophrenia by contributing to presynaptic dopamine abnormalities. Thus, we are examining inflammatory markers in dopaminergic areas of the midbrain of people with schizophrenia and matched controls.
Cognitive deficits play a major role in the disability and poor quality of life of people with schizophrenia (e.g. inability to study or work, difficulty maintaining social relationships), and schizophrenia results in more than $3 billion in health-related costs in Australia annually. In clinical practice, there are no effective treatments for the cognitive deficits in schizophrenia. In a recent clinical trial the Schizophrenia Research Laboratory identified that a selective estrogen receptor modulator, raloxifene enhanced cognition in some people with schizophrenia. The precise mechanism whereby raloxifene enhances cognition is not clear.
This project aims to uncover the molecular and cellular mechanisms of action of raloxifene and the behavioural correlates that are improved by raloxifene in healthy rodents and in rodents with a schizophrenia-like phenotype. This will aid in prioritising downstream molecular targets to develop novel treatments aimed at reversing or preventing the MIA-induced cognitive deficits. The ultimate goal is to translate this information to develop treatments for the debilitating cognitive deficits of schizophrenia.
In one of the biggest breakthroughs in schizophrenia research in recent times, Professor Cynthia Shannon Weickert’s research team have identified immune cells in greater amounts in the brains of some people with schizophrenia. The study published in the Journal of Molecular Psychiatry has the potential to transform global schizophrenia research and open new avenues for developing targeted immune cell therapies.
Studying the molecular basis of raloxifene (a SERM) modulation of dopamine signalling in schizophrenia, which uses a maternal immune activation rodent model of schizophrenia to better understand how raloxifene brings about its effects.
Together with Professor Peter Schofield (NeuRA) and Professor Philip Mitchell (Black Dog Institute), our group is investigating the genetic contributors to bipolar disorder using Australian families with multiple individuals who have been diagnosed with the disorder.
The group previously identified a bipolar susceptibility locus located on chromosome 15 in a pooled analysis of 35 families. More detailed analysis of this region has identified a single gene, which confers an increased susceptibility to both bipolar disorder and schizophrenia, and has also been implicated as a risk factor for autism.
The group is now aiming to understand how alterations in ST8SIA2 translate into an increased genetic susceptibility by characterising alterations in the DNA, RNA and protein product of this gene and its interaction partners in patients with either bipolar disorder or schizophrenia.
DEBORA ROTHMOND Senior Research Assistant
: 9399 1846