The neuronal correlates of reward and executive function interactions in adolescents with ADHD

Single causal pathway models of Attention-Deficit/Hyperactivity Disorder
(AD/HD) have emphasized deficits in executive function, primarily inhibitory
control. A substantial number of fMRI studies have focused on the neural basis
of inhibitory control in AD/HD and to lesser extent cognitive flexibility.
These studies show that AD/HD is associated with inefficient recruitment of
areas in prefrontal cortex, basal ganglia, and cerebellum during inhibitory
control tasks. However, accumulating evidence of considerable inter-individual
differences in executive function deficits in this disorder challenges this
view. In addition, fMRI studies on the neural basis of reward processing in
AD/HD have only just begun and generally show decreased ventral striatum
activation during reward processing in AD/HD. The neurotransmitter Dopamine has
been shown to play a crucial role in AD/HD. Medication to treat AD/HD symptomes
has its effect trough the Dopaminergic system. Dopamine Transporter (DAT)
genotype has been shown to determine indivudiual variations in Dopamine
baseline levels and affects the interaction between motivation and executive
controle in AD/HD.

Our current understanding of the heterogeneous nature of AD/HD has caused a
shift towards identifying multiple causal pathways. One influential example is
the dual pathway model which proposes that an executive function pathway and a
motivational pathway can each lead to symptoms of AD/HD. Although this model
has had a main impact and has prompted AD/HD researchers to study motivational
processes in addition to executive functions, there is a relative lack of
research that examines the conjunction of these two important pathways and no
fMRI research has studied the interaction between inhibitory control or
cognitive flexibility and reward/motivation in AD/HD.

Here we propose that in order to identify causal mechanisms that explain
AD/HD-related heterogeneity, an integrative approach is needed. Therefore, in
this project we will study the interaction between motivation and executive
function in AD/HD and the role of DAT genotype in these processes. More
specifically, we will study the bottom-up effects of motivation on inhibitory
control and cognitive flexibility in AD/HD as a function of DAT genotype. This
novel integrative approach will provide a more comprehensive account of the
mechanisms of this prevalent, complex disorder.

Aolescence is a critical period in life with an imbalance between motivation
and executive functioning. By including a substantial age range (12-17), and
balancing the AD/HD subtypes, we will be able to compare the developmental
trajectory of motivation-executive function interactions between AD/HD and
typically developing children.

controlled non-randomized observational intervention (MRI) study. Gender and
age will be balanced within groups.

There are no risks directly associated with this study. If applicable,
participants will have to discontinue psychostimulant medication. An
independent physician can be consulted at any time. Afterwards, participants
can continue their medication intake without harmful consequences. Risks
involved in MRI scans are neglible. To determine DAT genotype, a saliva sample
is taken. Also see reseach protocol for safety measures.