Dr Tertia Purves-Tyson

Raloxifene treatment in Maternal Immune Activation model of Schizophrenia

The role of the microbiome and metabolic syndrome in schizophrenia and related psychoses

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.

Increased levels of midbrain immune-related transcripts in schizophrenia: relationship to changes in

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.

Role of neuroinflammation and neurotransmitter systems in the improved cognition induced by estrogen

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.