+612 9399 1751
Current research focuses on the molecular/mechanistic understanding of how sex steroid signaling and neuroinflammation interact and contribute to striatal and cortical modulation of dopamine and how dopamine-related behaviours (psychotic-like symptoms, memory and cognition) are altered by sex steroids in male and female rats of different ages. The goal is to transfer this knowledge to human studies to develop or enhance sex steroid based and immune-related treatments for the cognitive and psychotic symptoms of schizophrenia in an age and gender-specific manner.
Dr Purves-Tyson completed a PhD at Manchester University, UK, implicating the mitogen-activated protein kinases in the aetiology of diabetic sensory neuropathy. She relocated to Australia in 2002 to investigate sex steroid signalling mechanisms in pelvic autonomic and sensory neurons. She was awarded an NHMRC Biomedical Training Fellowship and a Ramaciotti Foundation Establishment gift in 2004 to examine the effects of oestrogen on signalling mechanisms on the pelvic autonomic nervous system in diabetes.
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.
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.
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