Schizophrenia

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.

What is the purpose of the study?

We are interested in how the immune system influences the brain. We are seeking volunteer research participants to learn about how immune markers in the blood relate to cognition, behaviour and brain activity.

Would the research project be a good fit for me?

The study might be good for you if:

• You are between the ages of 18-60 and you are a healthy adult with or without a

sibling who has a diagnosis of schizophrenia or schizoaffective disorder

• You DO NOT have a personal history of schizophrenia, seizures, substance abuse or

dependence (within past 3 years), head injury or loss of consciousness, central nervous system infections

What would happen if I took part in the research project?

If you decide to take part you would visit Neuroscience Research Australia to complete the following:

• Perform cognitive tests and questionnaires (within 2 hours)
• Provide a blood sample
• Receive a short medical examination including a visual eye, nose, and throat exam,

lungs and heart (using stethoscope) exam, body temperature, blood pressure, and

brief medical history

• Receive an MRI scan (approx. 1 hr) which includes performing computer-based

cognitive tests

Will I be paid to take part in the research project?

Your participation in this study may have associated expenses. Reimbursement will be provided for your time and for out-of-pocket expenses, such as travel to the centre.

Who do I contact if I want more information or want to take part in the study?

If you would like more information or are interested in being part of the study please contact a member of our research team:

Alice Zhen on 02 9399 1858 email: a.zhen@neura.edu.au

Associate Professor Thomas Weickert on 02 9399 1730, email: t.weickert@neura.edu.au

A study of men and women between 18 to 70 years of age with a diagnosis of either melancholic or non-melancholic depression to research the extent to which blood biomarkers may be elevated in melancholic and non-melancholic subtypes of depression.

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.

The path to developing therapies to prevent schizophrenia involves research on how risk genes influence brain development and structure.

Since brain disease often involves neuronal death, research into strategies to restore neuronal numbers could lead to improved function and recovery in patients.

Canakinumab adjunctive treatment to reduce symptoms and improve cognition in people with schizophrenia displaying elevated blood inflammatory markers

This project aims to understand the bidirectional relationship between sleep and the brain to test and develop new approaches to treatment for sleep disruption across a range of medical disorders.  

This study tests the relationship among probabilistic association learning , schizotypal personality traits, striatal function and genes important to striatal function.

You are invited to participate in a research study using a human immune cell-line antibody to improve language, memory, and reduce symptoms of schizophrenia.

We are recruiting people with schizophrenia to take part in a study of the effects of transcranial Direct Current Stimulation (tDCS) upon thinking problems and some of the symptoms that occur with schizophrenia.