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AD 2 Disruption of brain connectivity in schizophrenia
  1. E Bullmore

Abstract

Ed Bullmore trained in clinical medicine at the University of Oxford and St Bartholomew's Hospital in London, then worked as a Lecturer in Medicine at the University of Hong Kong, before specialist clinical training in psychiatry at St George's Hospital and then the Bethlem Royal & Maudsley Hospital London. His research career started in the early 1990s as a Wellcome Trust Research Fellow and was initially focused on mathematical analysis of neurophysiological time series. Since moving to Cambridge as Professor of Psychiatry in 1999, his interest in systems-level analysis of brain function and structure has increasingly focused on using tools drawn from wavelet analysis and graph theory to investigate complex brain networks identified in human neuroimaging data (fMRI, MRI and MEG). Since 2005, he has worked half-time for GlaxoSmithKline as Head of GSK's Clinical Unit in Cambridge and Vice-President, Experimental Medicine. He is Deputy Director of the Wellcome Trust/GSK funded training programme in Translational Medicine and Therapeutics, Clinical Director of the Wellcome Trust/MRC funded Behavioural & Clinical Neuroscience Institute, and an honorary Consultant Psychiatrist and co-director of CAMEO in Cambridgeshire & Peterborough Foundation NHS Trust. He has published about 270 peer-reviewed articles and his h-index is 67.

The idea that schizophrenia reflects a disruption of brain connectivity dates back to the founding fathers of neuropsychiatry. Recent neuroimaging studies have provided fresh evidence for models of psychosis as disconnexion syndromes. I will review MRI studies of abnormal brain connectivity in schizophrenia with a focus on recent work using graph theory to measure the complex topological properties of human brain networks in healthy and psychotic individuals. These data clearly demonstrate abnormalities of the connectome in schizophrenia: they also raise questions for future research. In particular, how can we reconcile genetic and developmental models of pathogenesis with network abnormalities in schizophenia?

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