Relationship of DAT1 and adult ADHD to task-positive and task-negative working memory networks
Ariel Brown,Joseph Biederman,Eve M. Valera,Nikos Makris,Alysa E. Doyle,Susan Whitfield-Gabrieli,Eric Mick,Thomas J. Spencer,Stephen V. Faraone,Larry J. Seidman,Larry J. Seidman +10 more
TLDR
It is shown that DMN suppression is likely linked to DAT1 and to severity of inattention in ADHD, and may be a target of DAT2 effects, and lie on the path between the gene and inatt attention in ADHD.Abstract:
Alterations in working memory, default-mode network (DMN), and dopamine transporter have all been proposed as endophenotypes for attention-deficit/hyperactivity disorder (ADHD). Despite evidence that these systems are interrelated, their relationship to each other has never been studied in the context of ADHD. In order to understand the potential mediating effects of task-positive and task-negative networks between DAT1 and diagnosis, we tested effects of genotype and diagnosis on regions of positive and negative BOLD signal change (as measured with fMRI) in 53 adults with ADHD and 38 control subjects during a working memory task. We also examined the relationship of these responses to ADHD symptoms. Our results yielded four principal findings: 1) association of the DAT1 9R allele with adult ADHD, 2) marginal DAT1 association with task-related suppression in left medial PFC, 3) marginal genotype×diagnosis interaction in the dorsal anterior cingulate cortex, and 4) correlation of DMN suppression to ADHD symptoms. These findings replicate the association of the 9R allele with adult ADHD. Further, we show that DMN suppression is likely linked to DAT1 and to severity of inattention in ADHD. DMN may therefore be a target of DAT1 effects, and lie on the path between the gene and inattention in ADHD.read more
Citations
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Journal ArticleDOI
The genetics of attention deficit/hyperactivity disorder in adults, a review
Barbara Franke,Stephen V. Faraone,Philip Asherson,Jan K. Buitelaar,Claiton H.D. Bau,Josep Antoni Ramos-Quiroga,Eric Mick,Eugenio H. Grevet,Stefan Johansson,Stefan Johansson,Jan Haavik,Jan Haavik,K-P Lesch,K-P Lesch,Bru Cormand,Andreas Reif +15 more
TL;DR: Progress in identifying aADHD risk genes may provide tools for the prediction of disease progression in the clinic and better treatment, and ultimately may help to prevent persistence of ADHD into adulthood.
Journal ArticleDOI
Ventral–striatal responsiveness during reward anticipation in ADHD and its relation to trait impulsivity in the healthy population: A meta-analytic review of the fMRI literature
Michael M. Plichta,Anouk Scheres +1 more
TL;DR: It is concluded that at the present stage the number of existing studies in the healthy population as well as in ADHD groups is too small for a final answer and three theoretical approaches are discussed, each of which integrates the opposing findings.
Journal ArticleDOI
Attention-deficit/hyperactivity disorder (ADHD) and working memory in adults: a meta-analytic review.
TL;DR: Findings indicate that working memory deficits persist into adulthood and suggest that methodological variability may explicate why WM deficits have not been uniformly detected in previous experimental studies.
Journal ArticleDOI
Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies.
TL;DR: There were not enough genetic, pharmacogenetic and biochemical studies of ADHD in adults and that more investigations are needed, which confirmed a significant role of BAIAP2 and DHA in the etiology of ADHD exclusively in adults.
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A Review of Heterogeneity in Attention Deficit/Hyperactivity Disorder (ADHD)
TL;DR: A comprehensive review of the current status of research in understanding the heterogeneity of ADHD in terms of etiology, clinical profiles and trajectories, and neurobiological mechanisms suggests that further research focus on investigating the impact of the etiological risk factors and their interactions with developmental neural mechanisms and clinical profiles in ADHD.
References
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