Centre for Advanced Study

at the Norwegian Academy of Science and Letters

Attention-Deficit/Hyperactivity Disorder (ADHD) from genes to therapy


Former 2004/2005 Social Sciences - Law


The primary aim of the ADHD group at the Norwegian Centre for Advanced Study (CAS) will be to take advantage of the strong Norwegian neuroscience research community in bridging the present gap between basic and clinical research on Attention-Deficit/Hyperactivity Disorder (ADHD). Prior to the ADHD group at the Norwegian CAS, broad interdisciplinary collaboration between clinical researchers and basic neuroscientists on this disorder was largely nonexistent even on an international level. It will be the first time that an international interdisciplinary group has been gathered for trying to reach a comprehensive theory of ADHD.

It is expected that such a theory will form the basis, not only for future diagnosis and treatment of ADHD, but also for the design of future studies on animal and mathematical models that will be helpful in advancing the understanding of ADHD. Insights gained by the ADHD group at the Norwegian CAS will be disseminated in several ways, one of these is by organising an open international meeting in Norway at the end of the project (ultimo June 2005).

End Report

Attention-Deficit/Hyperactivity Disorder (ADHD) is a seemingly heterogeneous group of cognitive/behavioural developmental disorders where all clinical criteria are behavioural. ADHD affects between 2% and 12% of grade-school children. The disorder usually, but not always, manifests itself before the child is 7 years old. Of children diagnosed with ADHD, 50–70% will have problems related to social adjustment and functioning, and/or psychiatric problems as adolescents and young adults.

The primary aim of the CAS project was to combine behavioural and neuroscientific basic research on ADHD. The group represented the first, broad interdisciplinary collaboration between clinical researchers and basic researchers on ADHD anywhere in the world. The international interdisciplinary group had as its major objective to try to reach a thorough understanding of ADHD. To a large extent, this was obtained. All participants contributed to the new ways of looking upon ADHD.

As promised in the original application, the group worked on neurobiological data and insights that may bridge the present genetic and behavioural (clinical) evidence. The point of departure in the discussions and theory building was the neurobiology of the dopamine and glutamate systems, in particular the roles these systems play in neuronal plasticity, learning, and memory underpinning behavioural functions. The heterogeneous background of the group participants made possible the major advances in understanding some of the interactions involved. The insights form the main body of the application to the Norwegian Research Council submitted Sept 1st this year for funds for basic research on ADHD at the University of Oslo.

The main aim of this effort is further to strengthen basic research in Norway as stated in the overall goal of CAS. The advances made during this year would have been very difficult to obtain without researcher with a wide range of relevant backgrounds being gathered at a centre like CAS. Our new insights are now published in international journals and meetings. The new insights into ADHD will most likely form the basis, not only for future diagnosis and treatment of ADHD, but also for the design of future studies on animal and mathematical models that will be helpful in advancing the understanding of ADHD even further.

There is now general agreement that ADHD involves altered sensitivity to reinforcers (reward). A major achievement of the group is the realization that delay gradients results from pairing the reinforcer with the fading of precursors, for example, the fading of memory traces of the behaviour. Looking on delay gradients as expressions of underlying memory processes introduces novel perspectives into the dynamic developmental theory (DDT). Altering short-term or working memory of events may change effects of delayed reinforcers by increasing memorability of these events when the reinforcer is delivered. We now see how it will be possible to test this experimentally and how to investigate if this is related to a hypofunctioning dopamine system.

The DDT predicts that, at least early in training, there will be fewer units in a chain of behaviour in ADHD than normally. The slower acquisition of long behavioural chains will give rise to variable, less orderly behaviour that might appear impulsive. When we had worked out the underlying mathematics early this spring, we started to analyze data collected with children in Norway and South Africa, as well as with the validated animal model. The first of these publications is already published, and more will be submitted this autumn.

This is a major achievement with a substantial potential for designing new diagnostic instruments that may be used across cultures and languages. It might also explain why ADHD is associated with language problems, which typically involve sentences with many behavioural elements.

The DDT describes how the same etiological factor, changes in basic learning mechanisms, may produce a wide range of symptoms or behaviours depending on how these initial changes interact with the environment.

The DDT as further developed by the group at CAS, offers plausible explanations of a large number of ADHD behaviours both from a purely behavioural point of view and from a neurobiological (hypodopaminergic) point of view. Important areas for future studies include the relationship between reinforcement decay functions and memory, and between motor functions and timing in ADHD, as well as how initial neurobiological changes in ADHD affect long-term development. Also, advances in neuroscience will produce more precise knowledge about the neurobiological changes in ADHD. These insights will offer a more solid understanding of how altered neurobiological functions interacting with environmental factors produce ADHD symptoms.

We did not reach any conclusion on whether the hyperactive-impulsive and inattentive subtypes of ADHD are separate subgroups or may be explained as different outcomes of the same genetics and thus explained by the same principles.


  • Aase, Heidi
    Research Fellow Norwegian Institute of Public Health 2004/2005
  • Auerbach, Judith
    Associate Professor Ben-Gurion University 2004/2005
  • Banaschewski, Tobias
    Privat Dozent University of Göttingen 2004/2005
  • Berger, David F.
    Professor State University of New York at Cortland 2004/2005
  • Daley, David Michael
    Dr. University of Wales 2004/2005
  • Johansen, Espen BorgĂ„
    Research Fellow University of Oslo (UiO) 2004/2005
  • Killeen, Peter Richard
    Professor Arizona State University 2004/2005
  • Lombardo, John P.
    - State University of New York at Cortland 2004/2005
  • Meyer, Johanna Adelheid
    Professor University of Limpopo 2004/2005
  • Oades, Robert Duncan
    Professor University of Essen 2004/2005
  • Psychogiou, Lamprini
    Dr. University of Southampton 2004/2005
  • Russell, Vivienne Ann
    Professor University of Cape Town 2004/2005
  • Sergeant, Joseph Anthony
    Professor Vrije University 2004/2005
  • Sonuga-Barke, Edmund James
    Professor University of Southampton 2004/2005
  • Tannock, Rosemary
    Associate Professor University of Toronto 2004/2005
  • Tripp, Eileen Gail
    Dr. Okinawa Institute of Science and Technology 2004/2005
  • Wickens, Jeffery Russell
    Professor School of Medical Sciences 2004/2005
  • Williams, Jonathan Owen Heaton
    Dr. King's College London 2004/2005

Group leader

  • Terje Sagvolden

    Title Professor Institution University of Oslo (UiO) Year at CAS 2004/2005