Sophie completed a Bachelor of Science (Honours) at The University of Sydney in 2017. She completed her honours project at The Vascular Immunology Unit, where she examined how inflammation and microvesicles derived from brain endothelial cells contribute to the pathogenesis of cerebral malaria. Sophie has since worked as a Research Assistant at The Garvan Institute of Medical Research and as a Scientist at The Australian Red Cross Blood Service within the NSW Transplantation and Immunogenetics Laboratory. In 2019, Sophie joined NeuRA as a PhD candidate in the Schizophrenia Research Laboratory. Her PhD work involves investigating how dopamine dysregulation, neuroinflammation and stress-related genes contribute to the pathophysiology of schizophrenia.
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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Microvesicles and exosomes are implicated in cerebral malaria pathogenesis, in the modulation of host immunity to Plasmodium, and in cell-cell communication. Blocking their production is protective in models of cerebral malaria, both in vivo and in vitro.