Table 2 Functional neuroimaging-genetics studies in ADHD.

From: Genetic variations influence brain changes in patients with attention-deficit hyperactivity disorder

Genes

Index variants

Groups

MRI

Imaging matrix

Results

References

SLC6A3

9–6 SLC6A3 haplotype

9–6 haplotype carriers vs. non 9–6 haplotype carriers

fMRI

Rewarded and non‐rewarded trials

Bayesian Constraint-based Causal Discovery (BCCD) algorithm confirmed that there is no direct link between SLC6A3 genetic variability and brain activation, but suggested an indirect link mediated through inattention symptoms and diagnostic status of ADHD.

Sokolova et al.146

9‐6 SLC6A3 haplotype

SLC6A3 10–6 dosage (2 copies vs. <2 copies)

fMRI

VS and CN activity during reward-predicting cues

ADHD: activation in CN ↓ as a number of copies ↑, but in the control group reverse was found.

Paloyelis et al.143

3’ UTR VNTR

9R carriers vs. 10R/10R carriers

fMRI

Working memory task

9R carriers: ↓ left medial PFC activation compared to 10R/10R carriers. “Group × genotype interaction showed that 10R/10R-ADHD” “patients had ↑ activity in pre-SMA/dorsal ACC compared” to HC.

Brown et al.183

3’ UTR VNTR

10R/10R carriers vs. 9R carriers

fMRI

Go/No-Go task

10R/10R carriers: ↑ activity in frontal, medial, and parietal regions during response inhibition compared to 9R carriers; ↓error response in the parahippocampal gyrus.

Braet et al.184

3’ UTR VNTR

10R/10R carriers vs. 9R carriers

fMRI

Go/No-Go task

10R/10R carriers: ↑ activity in left striatum, right dorsal premotor cortex, and temporoparietal cortical junction compared to 9R carriers.

Bedard et al.144

3’ UTR VNTR

9R carriers vs. 10R/10R carriers

fMRI

Go/No-Go paradigm

9R carriers: ↑ activity in CN and ↓ in cerebellar vermis compared to 10R/10R carriers. Group × genotype interaction: effect in CN is observed in ADHD and unaffected siblings, but not HC.

Durston et al.185

3’ UTR VNTR

10R/10R carriers vs. 9R carriers

fMRI

Multi-source interference task

9R carriers: ↓ activity in dorsal ACC compared to 10R/10R carriers.

Brown et al.161

3’ UTR and intron 8 VNTR haplotype

9–6 haplotype carriers vs. non 9–6 haplotype carriers

fMRI

Striatal activity during reward anticipation task

No differences in striatal activity compared with non 9–6 haplotype carriers nor 9R- and 10R/10R carriers.

Hoogman et al.148

3’ UTR and intron 8 VNTR haplotype, rs37020, rs460000, rs4680

10–6 haplotype carriers vs. non-10–6 haplotype- carriers; rs37020

fMRI

Stop signal task

No genotype × ADHD interaction effects. SLC6A3 10–6 “haplotype-homozygotes: ↑ activity related to successful” stop-trials in pre-supplementary motor “areas, ↓ activity in superior frontal and temporal pole” areas. “rs37020 AA carriers: ↓ activity during failed stop-trials in IFG,” pre-supplementary motor areas, and postcentral gyrus.

van Rooij et al.158

COMT

rs4680

Met carriers vs. Val/Val carriers

rs-fMRI

Crus I/II in the cerebellum

Met-carriers exhibiting significantly lower functional connectivity than the Val/Val genotype.

Mizuno et al.160

SLC6A4

5-HTTLPR

3 genotype groups per variant

fMRI

Stop signal task

SLC6A4 SS-genotype group: ↓ activation in frontal nodes and “↑ activation in posterior nodes. No associations between SLC6A4 and HTR1B variants and ADHD or ADHD-related neural activation.

van Rooij et al.159

NOS1

exon 1f-VNTR

SS carriers vs. SL/LL carriers

fMRI

Reward anticipation task/modified MID task

SS carriers: ↑ activity in VS. No group × genotype interactions.

Hoogman et al.186

MAOA

rs1137070

TT carriers vs. CC carriers

fMRI

Working memory task

ADHD TT carriers: ↑ activation in the left inferior frontal lobe, pars opercularis.

Ko et al.147

HTR1B

5-HTTLPR, rs6296

3 genotype groups per variant

fMRI

Stop signal task

SLC6A4 SS-genotype group: ↓ activation in frontal nodes and “↑ activation in posterior nodes. HTR1B genotype: associated” with differential activation in anterior cingulate, occipital, inferior temporal, and cerebellar regions during successful stop trials. No associations between SLC6A4 and HTR1B variants and ADHD or ADHD-related neural activation.

van Rooij et al.159