Relationship of DAT1 and adult ADHD to task-positive and task-negative working memory networks
Open accessAbstract
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.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The DAT1 10/6 haplotype has been associated with ADHD in children, while the 9-repeat and 9/6 haplotype of DAT1 has been associated with persistent or adult ADHD.
“For example, the DAT1 10/6 haplotype has been associated with ADHD in children, while the 9-repeat and 9/6 haplotype of DAT1 was associated with persistent or adult ADHD (Franke et al., 2008; Brown et al., 2011).”
From A Review of Heterogeneity in Attention Deficit/Hyperactivity Disorder (ADHD) (2019) · cites this paper as Brown et al., 2011
The Discussion (page not provided) associates the DAT1 10-repeat allele with childhood ADHD and reports this study’s association of the 9-repeat allele with adult ADHD. The paper does not establish the more specific 10/6 or 9/6 haplotype associations, or an association specifically with persistent ADHD. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 67 · Cited by 53
- Authors
- Brown, A. B., Biederman, J., Valera, E., Makris, N., Doyle, A., Whitfield-Gabrieli, S., Mick, E., Spencer, T., Faraone, S., & Seidman, L.
- Affiliations
- Harvard University (US)
- SUNY Upstate Medical University (US)
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Brown, Ariel Beth
- ORCID
- Venue
- Psychiatry Research Neuroimaging
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 193
- Issue
- 1
- Pages
- 7-16
- ISSN
- 0925-4927 (ISSN-L)
- PMC
- PMC3105199
- OpenAlex
- W2038477622
- Cited by
- 53
- References
- 67
- Citations by year
- 2026: 1 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 4 · 2017: 2 · 2016: 3 · 2015: 6 · 2014: 6 · 2013: 4 · 2012: 9
- FWCI
- 4.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychiatry Research Neuroimaging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Eli Lilly and Company
- Shire
- Pfizer Pharmaceuticals
- National Institute of Mental Health (R01MH064019, MH-62152, K23MH071535, MH-071535, R01MH057934, MH-57934, MH64019, R01MH062152)
- National Center for Research Resources (P41-RR-14075, P41RR014075)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD036317, R01HD037694, HD36317, HD-37694)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- adult ADHD, dopamine transporter gene, default mode network, task-positive network, task-negative network, working memory, medial prefrontal cortex, dorsal anterior cingulate cortex, inattention, endophenotypes
- MeSH terms
- Adult, Analysis of Variance, Attention Deficit Disorder with Hyperactivity, Brain Mapping, Female, Genotype, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Memory Disorders, Memory, Short-Term, Middle Aged, Neuropsychological Tests, Oxygen, Prefrontal Cortex, Minisatellite Repeats, Dopamine Plasma Membrane Transport Proteins, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
