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Project

Delay Aversion in Adolescent Attention Deficit/Hyperactivity Disorder: Refining the Brain Endophenotype.

Attention Deficit/Hyperactivity Disorder is a common mental disorder of childhood with a poor prognosis, if not treated effectively. The current application focuses on delay aversion (DAv), an important altered motivational process in individuals with ADHD. Extensive behavioural evidence exists, supporting the DAv hypothesis as one important marker explaining ADHD individuals preference for small immediate rewards over larger delayed rewards. Within contemporary heterogeneic neuropsychological models of ADHD, DAv may represent one neurodevelopmental pathway explaining a substantial proportion of symptom variation. The neurobiological studies of this pathway in ADHD, so far, have mainly focused on altered brain responses to rewards, rather than to the anticipation or experience of delay as such. We recently published compelling results of a pilot study, applying functional neuro-imaging during an experimental task, developed in collaboration with Sonuga-Barke (who first formulated the DAv hypothesis) to index the motivational significance of DAv (i.e. the motivation to escape delay as a driver of an impulsive choice): the Escape Delay Incentive (EDI) task. In a small sample, we visualized brain activation effects for the impact of cues signaling inescapable delay and the opportunity to escape delay, independent from (monetary) reward cues, producing hyperactivation in brain regions sensitive to negative motivational affect (amygdala and insula) on trials with inescapable delay as opposed to escapable delay in the ADHD subjects compared to controls. The proposed three studies of the current project envisage to study the brain signature of DAv extensively. In study 1, we will add a control condition to the EDI and impose different levels of delay within the task. This will allow to dissociate the neural signature of reinforcing effects of delay escape and the punishing effects of delay imposition from each other and to establish a delay dose response curve. In study 2 we will contrast cues predicting various modes of delay to cues predicting modes of monetary rewards, in order to test the specificity of the neural delay activation pattern. Study 3 will investigate the neural processing of delay aversion and executive functioning in ADHD subjects by contrasting the EDI with a commonly used task shown to activate more dorsal executive networks (the Stop Signal Task of inhibitory control), thereby testing the dual pathway hypothesis. We hypothesize that these neural activation pathways will be dissociable from one another and that the separate neural activations will be correlated with performance on delay and executive function-related behavioural paradigms outside the scanner. Through these experiments we expect to provide a fundamental basis to the DAv dysfunction and to the dual pathway model in ADHD. Such fundamental understanding of the pathogenesis of ADHD will stimulate the development of targeted innovative treatments for this challenging disorder.
Date:1 Oct 2012 →  30 Sep 2016
Keywords:Endophenotype, ADHD, Adolescent
Disciplines:Biological and physiological psychology, General psychology, Other psychology and cognitive sciences