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Bronwyn Overs is a Research Assistant with a background in psychology. Her primary research interest is the genetic and neurological mechanisms of mental illness.
Bronwyn joined the Fullerton group in 2014 as part of the Bipolar Kids and Sibs study research team. This project investigates the biological and clinical features that increase the risk of developing bipolar disorder. As part of the research team she has applied a wide range of statistical models and analysis techniques to the exploration of genetic, brain imaging and neuropsychological data. Bronwyn is experienced in MRI image processing and editing, and has a passion for statistics and computer programming. Her work has contributed to the discovery of novel genetic and clinical markers that may identify individuals who are at increased risk of developing bipolar disorder and facilitate early intervention.
Bipolar Disorder is a highly heritable mood disorder characterised by oscillating periods of depression and mania. Previous research has established that this illness is accompanied by widespread changes in brain structure and function. However, the causes of these changes remain unknown. Are these changes a result of the illness process? Are they a product of the medications used to manage Bipolar symptoms? Do they represent the underlying cause of the clinical symptoms observed in this disorder? The Bipolar “Kids and Sibs” Study attempts to answer these questions by studying the young first-degree relatives of Bipolar Disorder patients, who are at increased risk of developing Bipolar Disorder or another related mental illness in the future themselves. As these young “at-risk” individuals have not received a Bipolar diagnosis and are free from medication, they provide a unique opportunity to examine brain differences that relate to both risk for and resilience to Bipolar Disorder.
The aim of this study is to identify neuroimaging biomarkers that may differentiate individuals who will ultimately go on to develop Bipolar Disorder or another mental illness, from individuals who are resilient and will remain well. This may assist in identifying those who are most at risk before they become unwell, and allow for interventions that prevent progression to illness or minimise the impact of this condition.
The offspring of individuals with bipolar disorder are at increased risk of mental illness, but our tools to predict which of these genetically at-risk young people will eventually develop disorder are very imprecise. Longitudinal studies that ascertain at-risk participants and monitor them prospectively are an effective approach for identifying early clinical and biological markers of future illness. In collaboration with the Black Dog Institute plus groups from four independent US-based sites, including: Johns Hopkins University; University of Michigan; Washington University in St. Louis; Indiana University; we are following a cohort of young kids and siblings of bipolar disorder patients with annual clinical, neurocognitive and lifestyle assessments; plus bi-annual brain imaging of the Australian participants. We are assessing the genetic load of multiple risk variants across the genome in these at-risk individuals to determine if we can use genetic information to help predict which individuals will ultimately transition to illness, and whether genetic load will influence early structural brain changes which are seen prior to onset of symptoms which lead to a clinical diagnosis.
We are also examining whether epigenetic changes – which occur on-top-of the DNA sequence in response to environmental influences – are involved in transition from health to illness. Early identification of those most likely to develop illness will provide a firm basis on which to develop preventive and early intervention strategies to reduce the impact of this devastating disorder.
In addition to genes identified in our own laboratory, we have also been involved in assessing the risk attributed by genes identified by other groups and in sharing data and samples in large international collaborative studies. We are contributors to the Psychiatric Genomics Consortium (PGC) and Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortia, which aim to identify risk genes which contribute to disease, and examine their effect on brain structure, function and disease.
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.
ANNA HEATH Research Assistant
KERRIE PIERCE Senior Research Assistant