Cognition to genes via the brain in the study of conduct disorder.
Although a single diagnostic label, conduct disorder, is currently applied to children exhibiting antisocial behaviour, multiple routes to the same behavioural phenomena exist. Morton and Frith's (1995) causal modelling has been fundamentally important in influencing models of cognitive/affective and associated neural differences between callous-unemotional (CU) and reactive/threat-based antisocial behaviour. Current behavioural genetic research is still catching up with the developmental cognitive neuroscience, and very few genetically informative studies differentiate between these two subtypes of antisocial behaviour. Our own work with preadolescent twins suggests that while the CU subtype is genetically vulnerable to antisocial behaviour, the non-CU subtype manifests a primarily environmental aetiology to their antisocial behaviour. Molecular genetic work to date has not differentiated between these two subtypes, and we highlight why it might be of interest to do so. Finally, we discuss how the novel approach of imaging genetics could be harnessed to study genes to cognition pathways for different subtypes of conduct disorder. Uta Frith's contributions to articulating research strategies for developmental disorders are important in conducting and interpreting this work.
Viding
Essi
E
Department of Psychology and Institute of Cognitive Neuroscience, University College London, London, UK. e.viding@ucl.ac.uk
Jones
Alice P
AP
D001321:Autistic Disorder / Q000453:epidemiology*; D001921:Brain / Q000503:physiopathology*; D002648:Child; D003072:Cognition Disorders / Q000453:epidemiology* / Q000503:physiopathology*; D019955:Conduct Disorder / Q000453:epidemiology* / Q000235:genetics*; D006801:Humans; D012938:Social Perception