Friston, K;
              
      
            
                Brown, HR;
              
      
            
                Siemerkus, J;
              
      
            
                Stephan, KE;
              
      
        
        
  
(2016)
  The dysconnection hypothesis (2016).
Schizophrenia research
, 176
       (2-3)
    
     pp. 83-94.
    
         10.1016/j.schres.2016.07.014.
  
  
       
    
  
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Abstract
Twenty years have passed since the dysconnection hypothesis was first proposed (Friston and Frith, 1995; Weinberger, 1993). In that time, neuroscience has witnessed tremendous advances: we now live in a world of non-invasive neuroanatomy, computational neuroimaging and the Bayesian brain. The genomics era has come and gone. Connectomics and large-scale neuroinformatics initiatives are emerging everywhere. So where is the dysconnection hypothesis now? This article considers how the notion of schizophrenia as a dysconnection syndrome has developed – and how it has been enriched by recent advances in clinical neuroscience. In particular, we examine the dysconnection hypothesis in the context of (i) theoretical neurobiology and computational psychiatry; (ii) the empirical insights afforded by neuroimaging and associated connectomics – and (iii) how bottom-up (molecular biology and genetics) and top-down (systems biology) perspectives are converging on the mechanisms and nature of dysconnections in schizophrenia.
| Type: | Article | 
|---|---|
| Title: | The dysconnection hypothesis (2016) | 
| Open access status: | An open access version is available from UCL Discovery | 
| DOI: | 10.1016/j.schres.2016.07.014 | 
| Publisher version: | http://dx.doi.org/10.1016/j.schres.2016.07.014 | 
| Language: | English | 
| Additional information: | © 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). | 
| Keywords: | Science & Technology, Life Sciences & Biomedicine, Psychiatry, Schizophrenia, Dysconnection, Neuromodulation, Bayesian, Predictive coding, Neurogenetics, NMDA RECEPTOR HYPOFUNCTION, 22Q11.2 DELETION SYNDROME, GENOME-WIDE ASSOCIATION, DE-NOVO MUTATIONS, MISMATCH NEGATIVITY, FUNCTIONAL CONNECTIVITY, PREFRONTAL CORTEX, MOUSE MODEL, FREE-ENERGY, CONNECTIONIST APPROACH | 
| UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Imaging Neuroscience | 
| URI: | https://discovery.ucl.ac.uk/id/eprint/1506355 | 
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