MAR 19, 2015 12:00 PM PDT
Special Lecturer - Towards a Neuroscience of Bipolar Disorder Risk
Presented at the Neuroscience Virtual Event
10 62 3051

Speakers:
  • Scientia Professor and Head of the School of Psychiatry, University of New South Wales
    Biography
      Philip Mitchell is Scientia Professor and Head of the School of Psychiatry at University of New South Wales in Sydney, Australia; Member, Australian National Health and Medical Research Council Research Committee; Vice-President (Governance), International Society for Bipolar Disorders; and Board Member, Black Dog Institute.

      His research and clinical interests are in bipolar disorder and depression, with a particular focus on: predictors of the development of bipolar disorder in at-risk individuals; molecular genetics of bipolar disorder; pharmacological and psychological treatments for bipolar disorder and depression; clinical phenomenology of bipolar disorder and depression; and neurostimulatory therapies for depression. Professor Mitchell has published over 450 peer-reviewed papers or book chapters and is lead investigator on an Australian NHMRC-funded Program Grant on depression and bipolar disorder. He serves on the editorial boards of ‘Psychiatric Genetics', ‘CNS Drugs', ‘CNS Spectrums', ‘Frontiers in Behavioral and Psychiatric Genetics', ‘Future Neurology', ‘International Journal of Bipolar Disorders', ‘Medicine Today' and ‘Therapeutic Advances in Psychopharmacology'.

      In 2002 he was awarded the Senior Research Award of the Royal Australian and New Zealand College of Psychiatrists (RANZCP). In 2004, he received the Founders Medal of the Australasian Society for Psychiatry Research. In 2008, he was invited to give the endowed Samuel Novey Lecture in Psychological Medicine at Johns Hopkins University, Department of Psychiatry and Behavioral Sciences. In the 2010 Australia Day honours list Professor Mitchell was appointed as a Member of the Order of Australia for service to medical education, particularly in the field of psychiatry, as an academic, researcher and practitioner, through contributions to the understanding, treatment and prevention of mental illnesses. In 2013 he was awarded the College Citation of the RANZCP for exceptional service to psychiatry.

    Abstract:
    There is growing interest internationally in elucidating the clinical and biological profile of those at high genetic risk to bipolar disorder (BD) so as to enable the development of targeted early intervention programs. This presentation will focus on the emerging findings from our group and others – highlighting both prospective and cross-sectional reports. Clinical studies are now converging in finding increased rates of both anxiety and behavioural disorders in this group, with three sites reporting that these disorders increase the risk of later development of affective disorders. Cross-sectional neuropsychological studies of first degree relatives of those with BD have previously suggested impairments in verbal learning and working memory, but prospective studies such as our own have not confirmed such findings, suggesting that the well-documented impairments in those with established BD may represent sequelae of the illness. Molecular genetic studies from our own work and a UK group have demonstrated an enrichment of BD polygenic risk alleles in young high risk individuals. Neuroimaging studies – both structural and functional – are now indicating differences compared to controls without any family history of mental illness. Our own initial fMRI study reported reduced inferior frontal gyrus (IFG) activation during response inhibition to emotional stimuli, suggesting a potential trait marker of vulnerability to BD. We have subsequently found, using dynamic causal modelling, that this impaired IFG activation appears to be due to a specific network disturbance suggesting dysfunction in the processes that support hierarchical relationships between emotion and cognitive control. Other groups have also reported functional and structural evidence implicating the IFG in those at high risk of BD. Our preliminary functional and structural (DTI) connectivity analyses are also indicating impaired connections between the IFG and other relevant brain regions.

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