Dopamine transporter genotype modulates brain activity during a working memory task in children with ADHD.
Kids with ADHD and the DAT1 9-repeat allele use more brain fuel to finish the same memory job as peers.
01Research in Context
What this study did
Researchers scanned the brains of 8- to young learners kids while they played a memory game.
Half the kids had ADHD; half were neurotypical.
The team also checked each child’s DAT1 gene to see if they carried the 9-repeat or 10-repeat version.
What they found
Kids with ADHD who had the 9-repeat allele lit up more brain areas during the game.
Their neurotypical peers with the same gene showed the opposite pattern—less activity.
Surprisingly, both groups scored the same on the memory test; only the brain effort differed.
How this fits with other research
Freeman et al. (2015) tracked memory growth for two years and saw ADHD kids slowly catch up, even though their brains still work harder.
Airoldi et al. (2025) explain that genes like DAT1 are only one layer; adding other ‘omics’ data can sharpen our picture.
Together, the papers say: same behavior can hide different brain roads—genes help us see the detours.
Why it matters
You can’t see a child’s DAT1 allele during a session, but you can watch for extra effort cues—fidgeting, sighs, long pauses. When you spot them, offer shorter work chunks or added breaks; the brain is doing heavy lifting even if the answers look easy.
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02At a glance
03Original abstract
Dopamine active transporter gene (DAT1) is a candidate gene associated with attention-deficit/hyperactivity disorder (ADHD). The DAT1 variable number tandem repeat (VNTR)-3' polymorphism is functional and 9R carriers have been shown to produce more DAT than 10R homozygotes. We used functional magnetic resonance imaging (fMRI) to investigate the effects of this polymorphism on the neural substrates of working memory (WM) in a small but selected population of children with ADHD, naïve of any psychotropic treatment and without comorbidity. MRI and genotype data were obtained for 36 children (mean age: 10,36 +/- 1,49 years) with combined-type ADHD (9R n = 15) and 25 typically developing children (TDC) (mean age: 9,55 +/- 1,25 years) (9R n = 12). WM performance was similar between conditions. We found a cross-over interaction effect between gene (9R vs. 10R) and diagnosis (TDC vs. ADHD) in the orbito-frontal gyrus, cerebellum and inferior temporal lobe. In these areas, WM-related activity was higher for 9R carriers in ADHD subjects and lower in TDC. In ADHD children only, 10R homozygotes exhibited higher WM-related activity than 9R carriers in a network encompassing the parietal and the temporal lobes, the ventral visual cortex, the orbito-frontal gyrus and the head of the caudate nucleus. There was no significant results in TDC group. Our preliminary findings suggest that DAT1 VNTR polymorphism can modulate WM-related brain activity ADHD children.
Research in developmental disabilities, 2019 · doi:10.1016/j.ridd.2019.103430