HIGHLIGHTS

• The link between divergent thinking and ADHD might depend on the impairment associated with ADHD.

• ADHD is not associated with increased convergent thinking.

• Psychostimulants do not have a negative effect on creativity as is often believed.

• Neuroscience of ADHD and creativity points to overlapping mechanisms.

• Evidence on strengths of ADHD is relevant because this may lead to increasing the self-views and quality of life of people with ADHD.

ABSTRACT

Attention deficit/hyperactivity disorder (ADHD) is a debilitating disorder and most research therefore focuses on its deficits and its treatment. Research on the potential positive sides of ADHD is limited, and although a comprehensive overview of empirical studies on this subject is missing, it has been suggested that ADHD is associated with enhanced creativity. To identify important relations, trends and gaps in the literature, we review 31 behavioral studies on creativity and ADHD, distinguishing different research designs, age groups, creativity measurements and effects of psychostimulants, as well as reflecting the potential underlying neural mechanisms of creativity and ADHD. Most studies find evidence for increased divergent thinking for those with high ADHD scores (subclinical) but not for those with the disorder (clinical). The rates of creative abilities/achievements were high among both clinical and subclinical groups. We found no evidence for increased convergent thinking abilities in ADHD, nor did we find an overall negative effect of psychostimulants on creativity. Neuroscientific findings suggest candidate regions as well as mechanisms that should be studied further to increase our understanding of the relationship between creativity and ADHD. We propose research opportunities to boost the knowledge needed to better understand the potential positive side of ADHD.

Abstract

Intolerance of uncertainty (IU), the tendency to find uncertainty negative, is a fundamental transdiagnostic dimension across anxiety-related disorders. Over the past two decades, there has been an increase in both clinical and experimental research on the role of IU in the maintenance and treatment of anxiety-related disorders. However, there has been a lack of integration of research findings from a mechanistic perspective, which has slowed progress in translational research. This review seeks to fill this gap by synthesising the clinical (e.g. randomised controlled trials) and experimental (e.g. lab-based) literature on the psychological mechanisms that drive change in IU across anxiety-related disorders. The review highlighted that: (1) cognitive restructuring, supported by mechanisms such as cognitive appraisal, modify IU-related cognitions, (2) behavioural exposures, supported by mechanisms such as inhibitory learning, alter IU-related cognitions and physiological arousal, and (3) mindfulness techniques underpinned by mechanisms such as attentional monitoring, decentering, and acceptance, change IU-related cognitions. Across the different therapeutic techniques reviewed, there was a lack of evidence for how different mechanisms change IU-related emotions and behaviours. Directions for further research include directly comparing the effectiveness of different mechanisms that produce change in IU across anxiety disorders and other mental health disorders, and examining the specificity of change in IU over other anxious traits. Overall, the findings provide a foundation for future translational research efforts to build upon maximising existing treatment interventions and/or to develop novel treatment interventions to target dispositional IU and situational uncertainty-related distress in anxiety-related disorders and beyond.

Highlights

• Intolerance of uncertainty (IU) is a fundamental transdiagnostic dimension.

• Review of clinical and basic research to identify mechanisms that change IU.

• Cognitive reappraisal modifies IU-related cognitions.

• Inhibitory learning alters IU-related cognitions and physiological arousal.

• Attentional monitoring, decentering, and acceptance change IU-related cognitions.

• Future translational research must isolate and compare mechanisms that alter IU.

Highlights

• Immediate early gene Arc expression is crucial for animal learning and memory.

• Learning-induced Arc mRNA and protein accumulate at dendrites and play a role in long-term synaptic plasticity.

• Arc has a viral origin, is capable of forming capsid-like structures and can transfect neighboring cells with its own mRNA.

• This Arc features raise new intriguing questions about the role of this traffic in neuronal plasticity and memory formation.

• The ability of Arc to form functional capsid-like structures can be used to develop new research and therapeutic tools.

Stabilization of neuronal plastic changes is mediated by transient gene expression, including transcription of the activity-regulated cytoskeleton-associated gene (Arc), also known as Arg 3.1. Arc is implicated in several types of synaptic plasticity, including synaptic scaling, long-term potentiation, and long-term depression. However, the precise mechanisms by which Arc mediates these forms of long-term plasticity are unclear. It was recently found that Arc protein is capable of forming capsid-like structures and of transferring its own mRNA to neighboring cells. Moreover, Arc mRNA undergoes activity-dependent translation in these “transfected” cells. These new data raise unexpected possibilities for the mechanisms of the Arc action, and many intriguing questions concerning the role of Arc transcellular traffic in neuronal plasticity. In this mini-review, we discuss a possible link between the role of Arc in learning and memory and the virus-like properties of this protein. Additionally, we highlight some of the emerging questions for future neurobiological studies and translational applications of Arc transsynaptic effects.