The DOI matches its Crossref record; 66 of the 69 references it cites were found in a registry or an index; none of the 39 sources its claims cite is checked for support yet.
Evaluating Dopamine Reward Pathway in ADHD: Clinical Implications
Open accessAbstract
We used positron emission tomography to measure dopamine synaptic markers (transporters and D2/D3 receptors) in 53 nonmedicated adults with ADHD and 44 healthy controls. For both ligands, statistical parametric mapping showed that specific binding was lower in ADHD than in controls in regions of the dopamine reward pathway in the left side of the brain. The mean for DAT in the nucleus accumbens for controls was 0.71 vs 0.63 for those with ADHD and in the midbrain for controls was 0.16 vs 0.09 for those with ADHD. For D2/D3 receptors, the mean in the caudate for controls was 2.80 vs 2.67 for those with ADHD; and in the accumbens for controls was 2.85 vs 2.68 for those with ADHD.
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22 Sources not found · 17 Own result · 12 Own method · 9 Own interpretation · 1 No basis given
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In the paper
“for D2/D3 receptors, the mean accumbens for controls was 2.85 vs 2.68 for those with ADHD (95% CI, 0.06–0.30, P=.004)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
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In the paper
“differences in D2/D3 in the hypothalamic region, with controls having a mean of 0.12 vs 0.05 for those with ADHD (95% CI, 0.02–0.12; P=.004)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
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In the paper
“but the reductions in left hypothalamic region were not significantly different (Table 2).”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine Transporters
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“and in the midbrain for controls was 0.16 vs 0.09 for those with ADHD (95% CI, 0.03–0.12; P ≤ .001)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“and in the midbrain, it was for controls 0.28 vs 0.18 for those with ADHD (95% CI, 0.02–0.17, P=.01)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The correlations with reflectivity or impulsivity and the PET dopamine measures were not significant”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
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In the paper
“However, despite this limitation, significant differences in the latter regions between controls and participants with ADHD was shown.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
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In the paper
“For both ligands, statistical parametric mapping showed that specific binding was lower in ADHD than in controls (threshold for significance set at P<.005) in regions of the dopamine reward pathway in the left side of the brain.”
- Also stated in: § Dopamine D2/D3 Receptors · plain
“Statistical parametric mapping analysis of the [11C]raclopride distribution volume ratio images revealed 1 cluster with lower D2/D3 availability in ADHD participants than controls in the left hemisphere.”
- Also stated in: § Dopamine Transporters · plain
“Statistical parametric mapping analysis of the [11C]cocaine distribution volume ratio images revealed a cluster in the same location as manifested in the [11C]raclopride images.”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
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- Also stated in: § Dopamine D2/D3 Receptors · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mean (95% CI for mean difference) of the K1 measures for [11C]cocaine did not differ in the left caudate with 0.49 among the controls vs 0.48 among those with ADHD (95% CI, −0.05 to 0.03) or in left accumbens region with a respective difference of 0.49 vs 0.51 among those with ADHD (95% CI, −0.02 to 0.07).”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine Transporters
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast the K1 measures for [11C]raclopride (transport of radioligand from plasma to tissue) did not differ either in left caudate with the both groups having a mean 0.11 (95% confidence interval [CI], −0.01 to 0.006 mean difference) or in left accumbens region with the controls having a mean of 0.12 vs a mean of 0.11 for those with ADHD (95% CI, −0.01 to 0.005).”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine D2/D3 Receptors
plain- Asserted: passes — The authors put it forward as true.
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- The quote only partly states this claim. 1
- Probably not a substantial claim. 18
- It may state two separate claims as one. 12
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There were no regions that were higher in ADHD participants than in controls.”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine D2/D3 Receptors
plain- Asserted: passes — The authors put it forward as true.
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The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and with DAT in the midbrain (r=0.37; 95% CI, 0.16–0.53; P ≤ .001).”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Lower than normal D2/D3 receptors and DAT availability in ADHD in the caudate was also demonstrated.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Genetic and environmental etiologies that implicate the neurotransmitter dopamine have been proposed for ADHD.3”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [3]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“The psychometric properties of the SWAN rating scale are superior to those of truncated symptom-severity ratings scales.22”
§ Evaluating Dopamine Reward Pathway in ADHD > METHODS > Clinical Scales
What the sources say
- Not matchedcites [22]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, this finding is preliminary and in need of replication.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“which could reflect that the scores were low and thus the sensitivity to observe such a correlation was lacking.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The preliminary finding reported herein of lower than normal dopamine D2/D3 receptor availability in the hypothalamic region of ADHD participants is intriguing because if replicated, it could hypothetically provide a neurobiological basis for the high co-morbidity of ADHD with signs and symptoms suggestive of hypothalamic pathology45 such as sleep disturbances,46 overweight or obesity,47 and abnor”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“the laterality effects should be interpreted as preliminary and in need of replication.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
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Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This study was not initially designed to evaluate hypothalamic dopamine involvement in ADHD.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Evidence from brain imaging studies have shown that brain dopamine neurotransmission is disrupted in ADHD5–9 and that these deficits may underlie core symptoms of inattention8 and impulsivity.9”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [6]
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- Not matchedcites [7]
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- Not matchedcites [8]
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- Not matchedcites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Morphological MRI images were not obtained and thus whether volumetric differences in striatum in those with ADHD that could account for these findings could not be ascertained since volumetric differences in striatum have been reported in ADHD.36–40”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
What the sources say
- Not matchedcites [36]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [37]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [38]
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- Not matchedcites [39]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [40]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In our study, the D2/D3 receptor measures in accumbens were correlated with the dimension of attention, which would implicate the dopamine reward pathway in the symptoms of inattention in ADHD.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“This pathway plays a key role in reinforcement-motivation and in learning stimuli-reward associations,51 and its involvement in ADHD supports the use of interventions to enhance the saliency of school and work tasks to improve performance.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [51]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
- Not matched
In the paper
“This rating system has been widely used in clinical and research settings and has well-established factor structure, reliability, and validity (Table 1).24”
§ Evaluating Dopamine Reward Pathway in ADHD > METHODS > Clinical Scales
What the sources say
- Not matchedcites [24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosted- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“The reward deficits in ADHD are characterized by a failure to delay gratification, impaired response to partial schedules of reinforcement, and preference for small immediate rewards over larger delayed rewards.31”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [31]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
In the paper
“Finally, because a low number of dopamine D2/D3 receptors in the nucleus accumbens have been associated with a greater risk for drug abuse,33 future work should determine if the lower than normal D2/D3 receptor availability in the accumbens region in ADHD underlies the higher vulnerability for substance abuse in this population.34”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [33]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
- Not matched
In the paper
“Both motivational interventions and contingency management have been shown to improve performance in ADHD patients.52”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [52]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Another study limitation was that measures of reward sensitivity were not performed. Thus, we can only infer that the decreases in the dopamine markers in the accumbens region could underlie the reward deficits that have been reported in patients with ADHD.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Multiple hypothalamic nuclei express dopamine D2 receptors,49 but the limited spatial resolution of a PET scan does not allow for localizing where the differences between the groups occurred.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [49]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“low statistical power may have contributed to the lack of significant ADHD-normal differences in the right brain regions.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Definitions for significant difference for the outcome measures1 were that statistical parametric mapping comparisons for the DAT and the D2/D3 images had to be significant at P<.005 (cluster corrected > 100 voxels) and the regional findings had to be corroborated by independently drawn region of interests2; comparisons for these corroborative measures had to be significant at P<.053; correlations”
§ Evaluating Dopamine Reward Pathway in ADHD > METHODS > Image Analysis and Statistics
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“The mesoaccumbens dopamine pathway, which projects from the ventral tegmental area (VTA) in the midbrain to the nucleus accumbens is critically involved in reward and motivation14 and has been hypothesized to underlie the reward and motivational deficits observed in ADHD.11,15”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [14]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [11]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [15]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Not matched
In the paper
“Alternatively it could reflect the involvement of frontal regions in impulsivity,57 which could not be measured with current PET radioligands; D2/D3 receptors and DAT levels in frontal regions are very low.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
What the sources say
- Not matchedcites [57]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: D2/D3 receptors and DAT levels in frontal regions are very low.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“There is also increased awareness that patients with ADHD may have reward and motivation deficits.10–12”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [10]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [11]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [12]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“but the limited spatial resolution of a PET scan does not allow for localizing where the differences between the groups occurred.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
No prior study has directly measured synaptic dopamine markers in the accumbens region of individuals with ADHD.
“However, to our knowledge no study has directly measured synaptic dopamine markers in the accumbens region of individuals with ADHD.”
The paper relies on this without support.
D2/D3 receptors and DAT levels in frontal regions are very low.
“D2/D3 receptors and DAT levels in frontal regions are very low.”
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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A number of studies have shown that ADHD is associated with a motivational deficit due to a dopamine dysfunction in the basal ganglia [71–73].”
From The brain anatomy of attention-deficit/hyperactivity disorder in young adults—a magnetic resonance imaging study (2017) · cites this paper as [71]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“using positron emission tomography (PET) we showed lower than normal availability of DA D2/D3 receptors (measured with [ 11 C]raclopride) and of DA transporters (measured with [ 11 C]cocaine) in the midbrain and in NAcc in drug naïve ADHD participants compared to non-ADHD control subjects 10 .”
From Motivation Deficit in ADHD is Associated with Dysfunction of the Dopamine Reward Pathway (2011) · cites this paper as [10]
In the citing paper
“As a number of researchers have described [106,149], substance-use disorders are typically accompanied by decreased reward motivation for typical and non-pathological rewards, a phenomenon that has been variously termed ‘motivational toxicity’ [150] and ‘reward-deficiency syndrome’ [151].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [149]
In the citing paper
“The immediate and marked response of ADHD symptoms to stimulant medications such as amphetamines and methylphenidate, which increase levels of synaptic dopamine, suggests that the main underlying pathophysiological process may involve deficits or imbalances in catecholaminergic, dopaminergic, and nicotinergic functioning [109-111].”
From European consensus statement on diagnosis and treatment of adult ADHD: The European Network Adult ADHD (2010) · cites this paper as [111]
In the citing paper
“It readily applies to ADHD because children with ADHD are at elevated risk of addiction, and both addiction and ADHD have been strongly associated with dysfunction in ascending dopaminergic systems that relate to reward response (Volkow et al., 2009, Volkow et al., 2011a, Volkow et al., 2011b).”
From Characterizing heterogeneity in children with and without ADHD based on reward system connectivity (2015) · cites this paper as Volkow et al., 2009
In the citing paper
“It readily applies to ADHD because children with ADHD are at elevated risk of addiction, and both addiction and ADHD have been strongly associated with dysfunction in ascending dopaminergic systems that relate to reward response (Volkow et al., 2009, Volkow et al., 2011a, Volkow et al., 2011b).”
From Characterizing heterogeneity in children with and without ADHD based on reward system connectivity (2015) · cites this paper as Volkow et al., 2009
In the citing paper
“Stimulant treatment, such as methylphenidate, is known to act directly on brain regions associated with disrupted dopamine reward pathways in ADHD [62,63] and may be responsible for the global effects seen with stimulant treatment in ADHD.”
From Will Working Memory Training Generalize to Improve Off-Task Behavior in Children with Attention-Deficit/Hyperactivity Disorder? (2012) · cites this paper as [63]
In the citing paper
“A subsequent study of ADHD subjects showed the same finding of reduced D2 receptor binding in the ventral striatum and caudate (Volkow et al., 2009), which correlated inversely with attention.”
From Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity (2014) · cites this paper as Volkow et al., 2009
In the citing paper
“Based on these results, this group hypothesized that decreased dopamine transmission plays a role in the motivation and reward deficits seen in ADHD, which are characterized by poor response inhibition and preference for small immediate rewards over larger delayed rewards (Volkow et al., 2009).”
From Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity (2014) · cites this paper as Volkow et al., 2009
In the citing paper
“Recent studies have further indicated deficits in the dopamine reward circuitry,3–5 as predicted by developmental neurobiological models of the disorder.6–8”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [5]
In the citing paper
“Neurochemical studies have demonstrated alterations in dopaminergic signaling in the striatum and the midbrain in ADHD, and linked such alterations with inattention symptoms and motivation problems in children and adults with ADHD.5,27–29”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [5]
In the citing paper
“A recent set of case–control PET studies in adult medication-naïve patients found that ADHD is associated with reduced dopamine transporter and dopamine D2/D3 receptor availability in selected brain regions of the left hemisphere, including the nucleus accumbens, caudate and midbrain (Volkow et al., 2007a, b, 2009).”
From A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment (2013) · cites this paper as Volkow et al., 2007a, b, 2009
In the citing paper
“This question is particularly relevant because findings for both juvenile and adult ADHD have implicated functional and structural midbrain abnormalities in the pathophysiology of the disorder (Ernst et al., 1999; Jucaite et al., 2005; Volkow et al., 2009; Romanos et al., 2010), also consistent with experimental animal models of ADHD (Leo et al., 2003).”
From A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment (2013) · cites this paper as Volkow et al., 2009
In the citing paper
“This result is consistent with previous evidence implicating the left caudate in inattentiveness, not only in patients with ADHD, but also in healthy subjects (Schrimsher et al., 2002; Volkow et al., 2007a, b, 2009) and is also congruent with reports that lesions in the left caudate produce attentional deficits (Benke et al., 2003).”
From A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment (2013) · cites this paper as Volkow et al., 2007a, b, 2009
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Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Correlation With ADHD Symptoms Dimensions
“The dimension of attention (from the SWAN) was negatively correlated with D2/D3 receptor availability in the left accumbens region (r=0.35; 95% CI, 0.15–0.52; P=.001)”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Correlation With ADHD Symptoms Dimensions
“Because the SWAN scale rates symptoms with a positive scale (from 1 to 3) and the opposite of symptoms with a negative scales (from −1 to −3) the negative correlation indicates that the lower the dopamine measures, the greater the symptoms of inattention.”
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“With PET imaging, lower D2/D3 receptor and DAT availability in those with ADHD than in the control group was documented in 2 key brain regions for reward and motivation (accumbens and midbrain).(29) It also corroborates disruption of synaptic dopamine markers in caudate in adults with ADHD and provides preliminary evi…”
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Items 301–400 of 726
Biomarkers for ADHD: the Present and Future Directions
Mehta, T., Mannem, N., Yarasi, N., & Bollu, P. C. (2020) · Current Developmental Disorders Reports · doi:10.1007/s40474-020-00196-9 · Cited by 20
Neurofeedback in ADHD: A qualitative study of strategy use in slow cortical potential training
Hasslinger, J., Souto, M. D., Folkesson, L., & Bölte, S. (2020) · PLoS ONE · doi:10.1371/journal.pone.0233343 · Cited by 21
Psychological Co-morbidities of Obesity
Pagoto, S., Schneider, K. L., Appelhans, B. M., Curtin, C., & Hajduk, A. M. (2011) · Springer eBooks · doi:10.1007/978-1-4419-0029-6_1 · Cited by 21
Application of MXene in the Electrochemical Detection of Neurotransmitters: A Review
Arjun, A. M., Shinde, M., & Slaughter, G. E. (2023) · IEEE Sensors Journal · doi:10.1109/jsen.2023.3285594 · Cited by 19
Schouw, M. L. J., de Ruiter, M. B., Kaag, A. M., van den Brink, W., Lindauer, R., & Reneman, L. (2012) · Drug and Alcohol Dependence · doi:10.1016/j.drugalcdep.2012.10.010 · Cited by 19
“Recreational dAMPH users did not have a significant response to MPH (positiv OI where a significant interaction of group × challenge was observed (Z > 2.3, p 0.05, clu of addicted individuals has been reported (for review see Volkow et al., 2009).”
InfluentialAttention Deficit Hyperactivity Disorder and Substance Use Disorders
Bukstein, O. G. (2011) · Current topics in behavioral neurosciences · doi:10.1007/7854_2011_148 · Cited by 19
García‐Yagüe, Á. J., & Cuadrado, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241512280 · Cited by 18
“The affected brain location, the Ventral Tegmental Area, exhibits a robust NURR1 expression [46,47].”
Neurotransmitter Imaging: Basic Concepts and Future Perspectives
Badgaiyan, R. D. (2011) · Current Medical Imaging Formerly Current Medical Imaging Reviews · doi:10.2174/157340511795445720 · Cited by 18
Riegler, A., Völkl-Kernstock, S., Lesch, O., Walter, H., & Skala, K. (2017) · Journal of Affective Disorders · doi:10.1016/j.jad.2017.03.072 · Cited by 20
Cherkasova, M., Faridi, N., Casey, K., Larcher, K., O'Driscoll, G., Hechtman, L., Joober, R., Baker, G., Palmer, J., Evans, A. C., et al. (2017) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2017.00421 · Cited by 16
“…disorder (ADHD) is thought to arise in part from alterations in catecholamine signaling (Castellanos et al., 1994; Spencer et al., 2005, 2013; Volkow et al., 2009; Cherkasova et al., 2014) and structural abnormalities in multiple cortico-striatal circuits (Nakao et al., 2011; Castellanos and…”
BackgroundMethyl-CpG-binding protein 2 mediates overlapping mechanisms across brain disorders
Bach, S., Ryan, N., Guasoni, P., Corvin, A. P., El-Nemr, R. A., Khan, D., Sanfeliu, A., & Tropea, D. (2020) · Scientific Reports · doi:10.1038/s41598-020-79268-0 · Cited by 20
“It is known that DA tracts also play a role in the aetiology of several neuropsychiatric diseases such as ASD, SCZ and ADHD (Volkow et al., 2009; Money and Stanwood, 2013) where many DA genes are disrupted.”
BackgroundShimada, K., Fujisawa, T. X., Takiguchi, S., Naruse, H., Kosaka, H., Okazawa, H., & Tomoda, A. (2015) · The World Journal of Biological Psychiatry · doi:10.3109/15622975.2015.1102325 · Cited by 18
“…data from various sources, including neuroimaging, genetic and pharmacological studies, have generally implicated deficits in dopaminergic fronto-striatal systems as the main cause of ADHD (Bush et al. 2005; Volkow et al. 2007; Gizer et al. 2009; Volkow et al. 2009; Bush 2010; Mizuno et al. 2013).”
BackgroundAttention Deficit Hyperactivity Disorder: A Mitigation of Criminal Responsibility?
Eme, R. F. (2014) · Journal of Forensic Psychology Practice · doi:10.1080/15228932.2014.923711 · Cited by 18
“The study found a markedly reduced number of receptors for the neurotransmitter dopamine in certain parts of the brain reward system that thereby reduced the ability to respond to rewards that are typically sufficient to activate and sustain motivation for those without ADHD (Volkow et al., 2009).”
BackgroundImpact and centrality of attention dysregulation on cognition, anxiety, and low mood in adolescents
Roberts, C., Sahakian, B. J., Chen, S., Sallie, S. N., Walker, C., White, S. R., Weber, J., Skandali, N., Robbins, T. W., & Murray, G. K. (2023) · Scientific Reports · doi:10.1038/s41598-023-34399-y · Cited by 25
Cascone, A., Calabro, F. J., Foran, W., Larsen, B., Nugiel, T., Parr, A. C., Tervo‐Clemmens, B., Luna, B., & Cohen, J. R. (2023) · Developmental Cognitive Neuroscience · doi:10.1016/j.dcn.2023.101274 · Cited by 18
“Studies of the neural etiology of response inhibition deficits in ADHD have focused on the neurotransmitter dopamine, given its established role in modulating frontostriatal circuits important for response inhibition (Fusar-Poli et al., 2012; Haber & Knutson, 2010; Nieoullon, 2002; Volkow et al., 2009).”
Salatino‐Oliveira, A., Genro, J. P., Chazan, R., Zeni, C., Schmitz, M. D., Polanczyk, G. V., Roman, T., Rohde, L. A., & Hutz, M. H. (2012) · Genes Brain & Behavior · doi:10.1111/j.1601-183x.2012.00835.x · Cited by 18
“Evidence from several neurobiological studies supports the idea that dysregulation of the catecholaminergic systems underlies ADHD neurobiology (Genro et al. 2010; Volkow et al. 2009).”
BackgroundStein, M. A., Waldman, I. D., Newcorn, J. H., Bishop, J. R., Kittles, R. A., & Cook, E. H. (2014) · Journal of Child and Adolescent Psychopharmacology · doi:10.1089/cap.2013.0102 · Cited by 17
“The issue of poor therapeutic response has recently been discussed by Volkow and colleagues (Volkow et al. 2009), who suggested that nonresponse to MPH may reflect very low dopamine activity while some adverse events may be the result of high neuronal activity.”
Self-citationAcute total sleep deprivation potentiates cocaine-induced hyperlocomotion in mice
Berro, L. F., dos Santos, R. A., Hollais, A. W., et al. (2014) · Neuroscience Letters · doi:10.1016/j.neulet.2014.07.028 · Cited by 17
Prevention of serious conduct problems in youth with attention deficit/hyperactivity disorder
Villodas, M. T., Pfiffner, L. J., & McBurnett, K. (2012) · Expert Review of Neurotherapeutics · doi:10.1586/ern.12.119 · Cited by 20
Punzi, M., Gili, T., Petrosini, L., Caltagirone, C., Spalletta, G., & Sensi, S. L. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00085 · Cited by 17
“…modafinil has also been clinically tested to treat cognitive dysfunctions often associated with the Attention Deficit/Hyperactivity Disorder (ADHD; Volkow et al., 2009), mood disorders (Goss et al., 2013), schizophrenia (Dawson et al., 2012), fatigue in multiple sclerosis (Kraft and Bowen, 2005),…”
BackgroundQuansah, E., & Zetterström, T. (2019) · Neurochemistry International · doi:10.1016/j.neuint.2019.01.016 · Cited by 17
Normalization of increased retinal background noise after ADHD treatment: A neuronal correlate
Werner, A. L., van Elst, L. T., Ebert, D., Friedel, E. B. N., Bubl, A., Clement, H., Lukačin, R., Bach, M., & Bubl, E. (2019) · Schizophrenia Research · doi:10.1016/j.schres.2019.04.013 · Cited by 18
Faltraco, F., Palm, D., Uzoni, A., Borchert, L., Simon, F. A. J., Tucha, O. M., & Thome, J. (2021) · Journal of Neural Transmission · doi:10.1007/s00702-021-02374-4 · Cited by 18
“Restless legs syndrome and attention deficit hyperactivity disorder (ADHD) are also associated with decreased dopamine activity (Guo 2017; Volkow 2009).”
BackgroundBidwell, L. C., Karoly, H. C., Hutchison, K. E., & Bryan, A. D. (2017) · Drug and Alcohol Dependence · doi:10.1016/j.drugalcdep.2017.06.020 · Cited by 18
“Given that dysfunction within dopaminergic systems is implicated in the pathophysiology of ADHD (Volkow et al., 2009), varenicline’s impact on striatal dopamine transmission (Di Ciano et al., 2016; Feduccia et al., 2014) may serve to reduce the severity of ADHD symptoms via facilitation of dopamine…”
BackgroundSweitzer, M. M., Kollins, S. H., Kozink, R. V., Hallyburton, M., English, J. S., Addicott, M. A., Oliver, J. A., & McClernon, F. J. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2017.248 · Cited by 17
“Individuals with ADHD are thought to exhibit altered dopamine transmission as evidenced by reduced dopamine D2/D3 receptor availability and attenuated dopamine receptor binding following MPH administration within the striatum and midbrain (Volkow et al, 2007, 2009).”
BackgroundInfluentialSelf-citationIs Attention-Deficit/Hyperactivity Disorder a Risk Syndrome for Parkinson’s Disease?
Baumeister, A. A. (2021) · Harvard Review of Psychiatry · doi:10.1097/hrp.0000000000000283 · Cited by 17
Sanches, E. S., Boia, R., Leitão, R. A., Madeira, M. H., Ribeiro, C., Ambrósio, A. F., Fernandes, R., & Silva, A. P. (2023) · Antioxidants · doi:10.3390/antiox12040937 · Cited by 16
“One of the hypotheses for ADHD etiology relies on the impairment in the dopaminergic system [41,42], and it is well established that dopamine plays a critical role in retinal function [43].”
BackgroundOhmori, I., Kawakami, N., Liu, S., Wang, H., Miyazaki, I., Asanuma, M., Michiue, H., Matsui, H., Mashimo, T., & Ouchida, M. (2014) · Epilepsia · doi:10.1111/epi.12750 · Cited by 17
“Brain imaging studies of patients with ADHD have shown disrupted neurotransmission of the mesolimbic DA reward pathway (projection from the VTA to the NA).(24,25) Midbrain dopaminergic neurons play a key role in cognition, motivation, reward, and regulation of coordinated movements.”
BackgroundArnett, A. B., Rhoads, C. L., & Rutter, T. M. (2021) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617721001065 · Cited by 19
“Neuroimaging studies have proposed novelty facilitates performance via frequent activation of dopaminergic reward pathways (Volkow et al., 2009).”
BackgroundGlymphatic system dysfunction in adult ADHD: Relationship to cognitive performance
Fang, Y., Peng, J., Chu, T., Gao, F., Xiong, F., & Tu, Y. (2025) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.03.059 · Cited by 16
Cardullo, S., Pérez, L. J. G., Cuppone, D., Sarlo, M., Cellini, N., Terraneo, A., Gallimberti, L., & Madeo, G. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2021.659527 · Cited by 16
Potts, Y., & Bekkers, J. M. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.919092 · Cited by 14
Mizuno, Y., Cai, W., Supekar, K., Makita, K., Takiguchi, S., Silk, T. J., Tomoda, A., & Menon, V. (2022) · Biological Psychiatry Cognitive Neuroscience and Neuroimaging · doi:10.1016/j.bpsc.2022.10.001 · Cited by 18
“Individuals with ADHD display low dopamine receptor availability in the corticolimbic pathway (5,6), and MPH has been hypothesized to ameliorate ADHD symptoms by increasing extracellular dopamine in the nucleus accumbens (NAc) (7).”
Waldie, K. E., Cornforth, C., Webb, R. E., Thompson, J., Murphy, R., Moreau, D., Slykerman, R. F., Morgan, A. R., Ferguson, L. R., & Mitchell, E. (2017) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.06.040 · Cited by 16
Methylphenidate alters monoaminergic and metabolic pathways in the cerebellum of adolescent rats
Quansah, E., Ruiz‐Rodado, V., Grootveld, M. C., & Zetterström, T. (2018) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2018.02.002 · Cited by 15
Marusich, J. A., McCuddy, W. T., Beckmann, J. S., Gipson, C. D., & Bardo, M. T. (2011) · Behavioural Pharmacology · doi:10.1097/fbp.0b013e32834d623e · Cited by 15
“Although the cause is not fully understood, research suggests that ADHD results from hypofunctioning dopaminergic systems (Sagvolden and Sergeant, 1998; Volkow et al., 2009).”
BackgroundVisual Attention in Flies—Dopamine in the Mushroom Bodies Mediates the After-Effect of Cueing
Koenig, S., Wolf, R., & Heisenberg, M. (2016) · PLoS ONE · doi:10.1371/journal.pone.0161412 · Cited by 15
“Both are known to have other targets besides dopamine [21, 24].”
BackgroundKapitansky, O., Giladi, E., Jaljuli, I., Bereswill, S., Heimesaat, M. M., & Gozes, I. (2020) · Journal of Neural Transmission · doi:10.1007/s00702-020-02155-5 · Cited by 15
Li, Y., He, Y., Wang, Y., He, J., Li, M., Wang, W.-Q., Wu, Z., Xu, Y.-J., He, W., Dou, Y.-L., et al. (2025) · World Journal of Pediatrics · doi:10.1007/s12519-025-00890-x · Cited by 15
“An increase in dopamine levels resulting from exercise interventions may be one mechanism to alleviate ADHD-related symptoms [46–48].”
Effects of auditory white noise stimulation on sustained attention and response time variability
Egeland, J., Lund, O., Kovalik-Gran, I., Aarlien, A. K., & Söderlund, G. B. W. (2023) · Frontiers in Psychology · doi:10.3389/fpsyg.2023.1301771 · Cited by 16
“In ADHD, the tonic and phasic regulation of dopamine in the brain has been especially studied, as tonic levels of dopamine are assumed to be low (Volkow et al., 2009), and that low tonic DA leads to higher phasic release (Seeman and Madras, 2002) in accordance with the tonic-phasic model of…”
ResultKubas, H. A., Backenson, E. M., Wilcox, G., Piercy, J. C., & Hale, J. B. (2012) · Postgraduate Medicine · doi:10.3810/pgm.2012.09.2592 · Cited by 14
“Additionally, recent longitudinal research found positive associations between medication use and standardized math and reading scores,(82) with positive longterm academic outcomes suggesting that MPH may increase the availability for learning through increased motivation, interest, and reward.(37) Despite evidence fo…”
BackgroundChu, C.-L., Lee, I. H., Chi, M. H., Chen, K. C., Chen, P. S., Yao, W. J., Chiu, N.-T., & Yang, Y. K. (2017) · CNS Spectrums · doi:10.1017/s1092852917000049 · Cited by 13
“Our results suggest that adults with ADHD have lower DAT levels than sex-, age-, and education-matched controls, and this is in line with the findings from studies with drug-naïve ADHD subjects.(21,22) Dopamine transporters were lower in both the caudate nucleus and putamen in ADHD adults than in controls.”
ResultRole of ADHD symptoms as a contributing factor to obesity in patients with MC4R mutations
Porfirio, M. C., Giovinazzo, S., Cortese, S., Giana, G., Lo‐Castro, A., Mouren, M., Curatolo, P., & Purper‐Ouakil, D. (2014) · Medical Hypotheses · doi:10.1016/j.mehy.2014.11.004 · Cited by 14
Le cerveau de l'hyperactif : entre cognition et comportement
Habib, M. (2011) · Développements · doi:10.3917/devel.009.0026 · Cited by 18
Noise benefit in prepulse inhibition of the acoustic startle reflex
Pålsson, E., Söderlund, G. B. W., Klamer, D., & Bergquist, F. (2010) · Psychopharmacology · doi:10.1007/s00213-010-2074-6 · Cited by 14
Adult ADHD: it is old and new at the same time – what is it?
Custodio, R. J. P., Hengstler, J. G., Cheong, J. H., Kim, H. J., Wascher, E., & Getzmann, S. (2023) · Reviews in the Neurosciences · doi:10.1515/revneuro-2023-0071 · Cited by 20
“Neuroimaging studies (Stevens et al. 2018; Volkow et al. 2009) revealed that distinct pathways are involved in speci fi c ADHD symptoms, including the involvement of the brain ’ s major dopaminergic systems, comprising the nigrostriatal, mesolimbic, mesocortical, and tuberoinfundibular systems that…”
BackgroundOzdemir, I., Arkın, H., Miloševıć, M. V., Barth, J. V., & Aktürk, E. (2024) · Surfaces and Interfaces · doi:10.1016/j.surfin.2024.104169 · Cited by 14
Neural basis for individual differences in the attention-enhancing effects of methylphenidate
Manza, P., Tomasi, D. G., Demiral, Ş. B., Kojori, E. S., Lildharrie, C., Lin, E., Wang, G., & Volkow, N. D. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2423785122 · Cited by 16
“This may be particularly beneficial in ADHD, a condition associated with aberrant levels of striatal D2/3 receptors ( 10 ), prefrontal D1 receptors ( 11 ), hypoactivity in the frontoparietal cortex during cognitive task performance ( 12 ), and disrupted functional connectivity between the dopamine…”
Self-citationMotor cortex modulation and reward in children with attention-deficit/hyperactivity disorder
Detrick, J. A., Zink, C. F., Rosch, K. S., Horn, P. S., Huddleston, D. A., Crocetti, D., Wu, S. W., Pedapati, E. V., Wassermann, E. M., Mostofsky, S. H., et al. (2021) · Brain Communications · doi:10.1093/braincomms/fcab093 · Cited by 14
Marois, A., & Lafond, D. (2022) · Cognition Technology & Work · doi:10.1007/s10111-022-00715-1 · Cited by 16
“Modafinil is a prescription drug for narcolepsy (Ballon and Feifel 2006; Volkow et al. 2009).”
BackgroundSderlund, G., & Sikstrm, S. (2012) · InTech eBooks · doi:10.5772/29657 · Cited by 13
“A hypo-functioning dopamine system is linked to inattention, and recent research suggests that ADHD possess low levels of extracellular dopamine (Solanto, 2002; Volkow et al., 2009; Volkow et al., 2007).”
BackgroundDopamine D3 receptor status modulates sexual dimorphism in voluntary wheel running behavior in mice
Klinker, F., Köhnemann, K., Paulus, W., et al. (2017) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.06.043 · Cited by 13
Dopamine and norepinephrine transporter inhibition for long-term fear memory enhancement
Pantoni, M. M., Carmack, S. A., Hammam, L., & Anagnostaras, S. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.112266 · Cited by 13
Cervini, P., Mattioli, I. A., & Cavalheiro, É. T. G. (2019) · RSC Advances · doi:10.1039/c9ra09046k · Cited by 13
Reinforcement learning modulates the stability of cognitive control settings for object selection
Sali, A. W., Anderson, B. A., & Yantis, S. (2013) · Frontiers in Integrative Neuroscience · doi:10.3389/fnint.2013.00095 · Cited by 15
“, and Franzel, S. L. (1989). Guided search: an alternative to the feature integration model for visual search.”
BackgroundNew Advances in Attention-Deficit/Hyperactivity Disorder-like Dogs
González‐Martínez, Á., de Miguel, S. M., & Diéguez, F. J. (2024) · Animals · doi:10.3390/ani14142067 · Cited by 17
“Participates in motor activity regulation and limbic functions, playing an essential role in attention and cognition, especially in executive functions [30] and reward processing [31].”
BackgroundWhy Don’t Smart Teens Have Sex? A Behavioral Genetic Approach
Harden, K. P., & Mendle, J. (2011) · Child Development · doi:10.1111/j.1467-8624.2011.01607.x · Cited by 12
“These genes might be mediated via dopaminergic neural circuits, which have been implicated in age at first sex (Miller et al., 1999), attentional disorders (Volkow et al., 2009), and animal models of cognitive abilities (Arnstein, Cai, Murphy, & Goldman-Rakic, 1994).”
Backgrounddel Campo, N., Tait, R. J., Acosta‐Cabronero, J., Hong, Y. T., Izquierdo‐Garcia, D., Smith, R., Aigbirhio, F. I., Sahakian, B. J., Müller, U., Robbins, T. W., et al. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2010.11.071 · Cited by 12
“Consistent with previous findings (Volkow et al., 2009; Volkow et al., 2007b), we found that high scores on a self-rating”
InfluentialNotes on the Role of the Cerebellum in ADHD
Goetz, M., Veselá, M., & Ptáček, R. (2014) · Cited by 14
Methylphenidate and Guanfacine Ameliorate ADHD-Like Phenotypes in Fez1-Deficient Mice
Sumitomo, A., Saka, A., Ueta, K., Horike, K., Hirai, K., Gamo, N. J., Hikida, T., Nakayama, K. I., Sawa, A., Sakurai, T., et al. (2017) · Complex Psychiatry · doi:10.1159/000488081 · Cited by 12
An Approach for Stabilizing Abnormal Neural Activity in ADHD Using Chaotic Resonance
Nobukawa, S., Wagatsuma, N., Nishimura, H., Doho, H., & Takahashi, T. (2021) · Frontiers in Computational Neuroscience · doi:10.3389/fncom.2021.726641 · Cited by 11
Grochecki, P., Smaga, I., Surówka, P., Marszałek‐Grabska, M., Kalaba, P., Dragačević, V., Kotlinska, P., Filip, M., Lübec, G., & Kotlinska, J. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810718 · Cited by 14
“Although results are mixed [74,75], ADHD patients are commonly treated with the DAT inhibitor, methylphenidate [76], although other DAT inhibitors, such as modafinil [77], were also clinically tested in ADHD.”
BackgroundMitchell, J. T., McIntyre, E., McClernon, F. J., & Kollins, S. H. (2013) · Nicotine & Tobacco Research · doi:10.1093/ntr/ntt144 · Cited by 12
“…and treatment. introDUction Attention-deficit/hyperactivity disorder (ADHD) is a disorder that arises in childhood and persists into adulthood in a majority of cases (Barkley, Murphy, & Fischer, 2008) and is characterized by fundamental deficits in motivational processes (Volkow et al., 2009).”
BackgroundSelf-citation“Turning Intentions Into Actions”: CBT for Adult ADHD Focused on Implementation
Ramsay, J. R. (2016) · Clinical Case Studies · doi:10.1177/1534650115611483 · Cited by 12
Diao, Y., Huang, Y., Zhu, B., Guo, M., Wang, W., Li, Z., Li, W., Zhang, H., Zhou, J., Li, X., et al. (2026) · Research · doi:10.34133/research.1115 · Cited by 12
Wu, F., Zhang, W., Ji, W., Zhang, Y., Jiang, F., Li, G., Hu, Y., Wei, X., Wang, S.-Y., Wang, S.-Y., et al. (2024) · Neuropsychopharmacology · doi:10.1038/s41386-024-01831-4 · Cited by 15
Self-citationLessons From the 1918 Flu Pandemic: A Novel Etiologic Subtype of ADHD?
Swanson, J. M., & Volkow, N. D. (2020) · Journal of the American Academy of Child & Adolescent Psychiatry · doi:10.1016/j.jaac.2020.09.024 · Cited by 11
Self-citationAydın, A. G., & Adıgüzel, E. (2023) · Laboratory Animal Research · doi:10.1186/s42826-023-00172-5 · Cited by 11
Özcan, K., Özcan, Ö., Muluk, N. B., Cingi, C., & Durukan, K. (2013) · International Journal of Pediatric Otorhinolaryngology · doi:10.1016/j.ijporl.2013.09.020 · Cited by 11
Separable Influences of Reward on Visual Processing and Choice
Soltani, A., Rakhshan, M., Schafer, R. J., Burrows, B. E., & Moore, T. (2020) · Journal of Cognitive Neuroscience · doi:10.1162/jocn_a_01647 · Cited by 11
“…be used to disambiguate neural mechanisms underlying attention and reward (Hikosaka, 2007; Maunsell, 2004, 2015), and how deficits in deployment of selective attention, which is characterized by changes in sensory processing, are affected by abnormalities in reward circuits (Volkow et al., 2009).”
BackgroundEffects of comorbid disorders on reward processing and connectivity in adults with ADHD
Grimm, O., van Rooij, D., Tshagharyan, A., Yildiz, D., Leonards, J., Elgohary, A., Buitelaar, J. K., & Reif, A. (2021) · Translational Psychiatry · doi:10.1038/s41398-021-01758-0 · Cited by 11
A Developmental Model of Self-Inflicted Injury, Borderline Personality, and Suicide Risk
Derbidge, C. M., & Beauchaine, T. P. (2014) · Springer eBooks · doi:10.1007/978-1-4614-9608-3_26 · Cited by 12
Neurotoxicity and Potential Mechanisms of Exposure to Per- and Polyfluoroalkyl Substances (PFASs)
Song, Y., Ma, Y., Huang, Y., Song, D., Hu, C., Zhang, X., Chen, Y., Zhang, L., & Lu, L. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05573-2 · Cited by 12
“ADHD is linked to dopamine dysfunction, with individuals exhibiting reduced dopamine synaptic markers in the reward pathway, which are associated with inattentiveness [131].”
Self-citationLongitudinal Smoking Patterns: Do They Predict Symptoms of ADHD in Adults?
Brook, J. S., Balka, E. B., Zhang, C., & Brook, D. W. (2015) · Journal of Attention Disorders · doi:10.1177/1087054715584057 · Cited by 10
“Volkow et al. (2009), using positron emission tomography (PET) scans, also studied the dopamine reward pathway in those with ADHD.”
MethodItagaki, S., Ohnishi, T., Toda, W., Sato, A., Matsumoto, J., Ito, H., Ishii, S., Yamakuni, R., Miura, I., & Yabe, H. (2024) · Psychiatry and Clinical Neurosciences Reports · doi:10.1002/pcn5.177 · Cited by 10
“9 DAT knockout mice exhibit altered decision ‐ making processes and motivational states as well as motor and oral stereotypies, 10,11 which are closely related to the pathophysiology of ADHD.”
BackgroundResultInfluentialPeña, P. Y., Riley, J., & Davis, N. L. (2024) · Marketing Education Review · doi:10.1080/10528008.2024.2337345 · Cited by 10
“The positive effects of dopamine have been well-documented, particularly in individuals with ADHD or attention span challenges (Volkow et al., 2009).”
BackgroundAhmad, S., Naveen, K. G., Babu, A. M., Ranjan, R., & Kumar, P. (2024) · Cureus · doi:10.7759/cureus.71527 · Cited by 15
Takım, U., Belli, H., Gökçay, H., Köse, H., Akgül, H. A., & Çakır, A. (2024) · ALPHA PSYCHIATRY · doi:10.5152/alphapsychiatry.2024.241630 · Cited by 10
“29,30 Notably, each of the aforementioned comorbid disorders is also linked to altered reward processing, as described recently.”
Aoki, S., Kaizaki‐Mitsumoto, A., Hattori, N., & Numazawa, S. (2021) · Toxicology Letters · doi:10.1016/j.toxlet.2021.02.016 · Cited by 12
Effects of Methylphenidate on the Dopamine Transporter and Beyond
Zetterström, T., Quansah, E., & Grootveld, M. C. (2022) · Current topics in behavioral neurosciences · doi:10.1007/7854_2022_333 · Cited by 11
Mayer, F. P., Stewart, A., Varman, D. R., Moritz, A. E., Foster, J. D., Owens, A. W., Areal, L. B., Gowrishankar, R., Velez, M., Wickham, K., et al. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03055-4 · Cited by 11
Caprioli, D., Fryer, T. D., Sawiak, S. J., Aigbirhio, F. I., & Dalley, J. W. (2013) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2013.04.003 · Cited by 10
Adult attention deficit hyperactivity disorder: translating research into practice
Coogan, A. N., Dobrean, A., Donev, R., Mateescu, L., Müller, U., Thome, J., & Voinescu, B. (2012) · ADHD Attention Deficit and Hyperactivity Disorders · doi:10.1007/s12402-012-0073-7 · Cited by 10
Koutsilieri, E., Riederer, P. F., du Plessis, S., & Scheller, C. (2014) · ADHD Attention Deficit and Hyperactivity Disorders · doi:10.1007/s12402-014-0134-1 · Cited by 12
Human Brain Imaging of Dopamine Transporters
Varrone, A., & Halldin, C. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-418677-4.00009-9 · Cited by 13
Zhou, M., Gresack, J. E., Cheng, J., Uryu, K., Brichta, L., Greengard, P., & Flajolet, M. (2018) · Molecular Psychiatry · doi:10.1038/s41380-018-0233-z · Cited by 10
Hai, T., Duffy, H. A., Lemay, J.-F., Swansburg, R. M., Climie, E. A., & MacMaster, F. P. (2020) · Europe PMC (PubMed Central) · Cited by 10
Porfirio, M. C., Lo‐Castro, A., Giana, G., Giovinazzo, S., Purper‐Ouakil, D., Galasso, C., & Curatolo, P. (2012) · Psychiatric Genetics · doi:10.1097/ypg.0b013e3283539604 · Cited by 9
“Current findings link both overweight/obesity and ADHD to the dopaminergic pathways and implicate dopamine genes in weight control, eating behaviors, and ADHD, among others (Cortese et al., 2008; Volkow et al., 2009).”
BackgroundAttention Deficit Hyperactivity Disorder
Swanson, J. M., Sergeant, J. A., Taylor, E. A., Sonuga-Barke, E. J. S., Jensen, P. S., & Castellanos, F. X. (2016) · Springer eBooks · doi:10.1007/978-1-4614-6434-1_169-1 · Cited by 10
Self-citationSeasonal variation of spontaneous blink rate and beta EEG activity
Barbato, G., Cirace, F., Monteforte, E., & Costanzo, A. (2018) · Psychiatry Research · doi:10.1016/j.psychres.2018.08.051 · Cited by 10
Linking the microarchitecture of neurotransmitter systems to large-scale MEG resting state networks
Siebenhühner, F., Palva, J. M., & Palva, S. (2024) · iScience · doi:10.1016/j.isci.2024.111111 · Cited by 9
Hilz, E. N., Schnurer, C., Bhamidipati, S., Deka, J., Thompson, L. M., & Gore, A. C. (2025) · Hormones and Behavior · doi:10.1016/j.yhbeh.2025.105697 · Cited by 8
“D2 receptor and dopamine transporter genes are implicated in the etiology of ADHD (DiMaio et al., 2003; Swanson et al., 2000; Volkow et al., 2009), and D2 specifically is implicated in hyperactivity (Fan et al., 2010).”
Obesity and Attention-Deficit Hyperactivity Disorder
Lanoye, A. M., Adams, E., & Fuemmeler, B. F. (2022) · Current topics in behavioral neurosciences · doi:10.1007/7854_2022_337 · Cited by 9
Cortico-striatal differences in the epigenome in attention-deficit/ hyperactivity disorder
Shastri, G. G., Sudre, G. P., Ahn, K., Jung, B., Kolachana, B. S., Auluck, P. K., Elnitski, L. L., Marenco, S., & Shaw, P. (2024) · Translational Psychiatry · doi:10.1038/s41398-024-02896-x · Cited by 11
Cumming, P. D., Caprioli, D., & Dalley, J. W. (2010) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2010.01036.x · Cited by 9
“A subsequent study of a larger cohort of never-medicated ADHD patients (n = 53) replicated the finding of reduced [11C]raclopride and [11C]cocaine binding in the left NAcb and caudate, which extended to the midbrain as well in this study (Volkow et al., 2009).”
ResultNa, K., Lee, S. I., Hong, S. D., Kim, J.-H., Shim, S.-H., Choi, J., Yang, J.-W., Lee, M., Joung, Y., Kim, E., et al. (2013) · International Clinical Psychopharmacology · doi:10.1097/yic.0b013e3283612509 · Cited by 9
“Also, methylphenidate plays an important role in the mesoaccumbens dopamine pathway, which is responsible for modulating reward and motivational responses (Volkow et al., 2009).”
Backgroundvan Langen, M. J. M., van Hulst, B. M., Douma, M., Steffers, M., van de Wiel, N. M. H., van den Ban, E. F., Durston, S., & de Zeeuw, P. (2020) · Journal of Attention Disorders · doi:10.1177/1087054720928136 · Cited by 9
“…likely involved; either through a general reduction of synaptic dopamine resulting in reduced sensitivity to delayed reward (Sagvolden et al., 2005; Volkow et al., 2009, 2011), or through what has been termed the dopamine transfer deficit, a reduced firing of dopamine cells in the ventral striatum…”
BackgroundLam, A. P., de Sordi, D., Müller, H., Lam, M. C., Carl, A., Kohse, K. P., & Philipsen, A. (2020) · Scientific Reports · doi:10.1038/s41598-020-71084-w · Cited by 11
Treatment with stimulants and the risk of COVID-19 complications in adults with ADHD
Tuan, W., Babinski, D. E., Rabago, D., & Zgierska, A. E. (2022) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2022.07.005 · Cited by 12
Magnetic Resonance Spectroscopy Studies of Attention Deficit Hyperactivity Disorder
O’Neill, J., Levitt, J. G., & Alger, J. R. (2012) · Springer eBooks · doi:10.1007/978-1-4419-5864-8_18 · Cited by 9
Metadata
- Authors
- Volkow, N. D., Wang, G.-J., Kollins, S. H., Wigal, T. L., Newcorn, J. H., Telang, F., Fowler, J. S., Zhu, W., Logan, J., Ma, Y., Pradhan, K., Wong, C., & Swanson, J. M.
- Affiliations
- National Institute on Drug Abuse (US)
- Corresponding author
- Volkow, Nora D.
- ORCID
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2009-09-09
- Volume
- 302
- Issue
- 10
- Pages
- 1084
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC2958516
- OpenAlex
- W2071411087
- Semantic Scholar
- 73303180da9a733fdf01dc78501b5769db289660
- Cited by
- 728
- References
- 69
- Citations by year
- 2026: 67 · 2025: 46 · 2024: 36 · 2023: 27 · 2022: 35 · 2021: 37 · 2020: 37 · 2019: 29 · 2018: 29 · 2017: 40 · 2016: 29 · 2015: 39 · 2014: 62 · 2013: 52 · 2012: 61
- FWCI
- 33.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (ZIAAA000550)
- National Institute of Mental Health (R01MH066961)
- National Institute on Drug Abuse (K24DA023464)
- 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
- attention deficit hyperactivity disorder, dopamine reward pathway, dopamine transporter, D2/D3 receptors, nucleus accumbens, caudate nucleus, adult ADHD, neuroimaging biomarkers, cocaine binding, left hemisphere lateralization, inattention, hyperactivity/impulsivity
- MeSH terms
- Adult, Attention Deficit Disorder with Hyperactivity, Brain, Brain Mapping, Carbon Radioisotopes, Cocaine, Dopamine, Female, Humans, Male, Mesencephalon, Synaptic Transmission, Reward, Dopamine Agents, Receptors, Dopamine D2, Raclopride, Positron-Emission Tomography, Dopamine Plasma Membrane Transport Proteins
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