ADHD and Dopamine
ADHD and Dopamine: Why a dopamine deficiency alone does not explain everything
ADHD and Dopamine: Why a dopamine deficiency alone does not explain everything
DESCRIPTION: The narrative of dopamine deficiency explains ADHD in a single sentence and has persisted for thirty years. What the major genome studies really show, and why the dopamine hypothesis has gaps.
ADHD and dopamine: Why a dopamine deficiency is not a sufficient explanation
The most common explanation for ADHD is: too little dopamine. It features in information leaflets, apps and millions of short videos. There is too little of this neurotransmitter in the ADHD brain; this is why there is a lack of drive, why people seek out stimuli, and why stimulants work, as they compensate for the deficiency.
However, large-scale genomic studies in recent years show that dopamine deficiency is not the sole cause of these behavioural and experiential patterns. Imaging studies provide even more contradictory results. The international consensus paper by experts does not describe ADHD as the result of such a deficiency. It is a model that aids understanding; it does not provide a complete explanation.
The image of an empty tank
This explanation has one obvious advantage: it fits into a single image. An empty tank. Too little fuel, too little drive, too much searching for the next stimulus. Medication fills the tank.
For many of those affected, this image serves a purpose:
· In practice, it offers a straightforward answer to a question that cannot otherwise be answered in five minutes.
· It takes the pressure off those affected by removing difficulties from the realm of moral judgement, such as lack of willpower, laziness, or character flaws.
· ‘Dopamine management’ helps with many problems associated with ADHD.
· But it also lends itself to digital self-optimisation, dietary supplements and focus-enhancing products, as it provides an intuitive problem-solving framework.
Where the idea came from
Researchers investigated whether certain variants of two genes occur slightly more frequently in ADHD. Both genes are associated with the dopamine system. However, the results were weak and inconsistent. Nevertheless, they gave rise to a plausible hypothesis: if dopamine plays a role in ADHD, variants in genes of the dopaminergic system could increase the risk.
At the time, meta-analyses identified isolated statistical associations. The 2009 meta-analysis by Gizer, Ficks and Waldman reported associations for DAT1, DRD4, DRD5 and other genes, whilst also noting considerable differences between the studies. Later and larger analyses showed significantly smaller effects.
In the case of a variant of the dopamine transporter gene DAT1, Grünblatt and colleagues found a very small statistical association with ADHD in children and adolescents. An odds ratio of 1.105 means that the variant was only slightly more common in those affected – not, for example, ‘ten per cent more ADHD’ and certainly not an indication of a causal link. This association was not observed in adults.
For a variant of the dopamine receptor gene DRD4, Bonvicini and colleagues found an association only in a specific group: children of European descent. Furthermore, they did not examine the same genetic loci as those investigated in the large, more recent genome-wide studies. Those studies found no association.
In short: individual variants in dopamine genes may be marginally associated with ADHD in some studies. However, they do not explain ADHD – and the results are too weak and too inconsistent to allow us to derive a simple narrative about the ‘dopamine gene’ or ‘dopamine deficiency’. Dopamine still plays a role in ADHD research. But the initial assumption that a few ‘dopamine genes’ explained ADHD did not stand up to scrutiny in larger sample sizes.
What the large-scale studies show
In 2019, researchers analysed the genetic data of more than 55,000 people – both with and without ADHD. They were not looking for a single ‘ADHD gene’, but rather for many small genetic differences that occur slightly more frequently in people with ADHD. In doing so, they identified 12 genetic loci statistically associated with ADHD.
In 2023, the researchers repeated the study with a much larger group: more than 225,000 people. This time, the researchers identified 27 such genetic loci and 76 genes that may be involved. Many of these genes are primarily active during the very early stages of brain development, including in areas of the frontal lobe important for planning, attention, and impulse control.
The key finding is this: ADHD cannot be attributed to a single gene, a specific area of the brain or a neurotransmitter such as dopamine. Rather, it involves many small genetic influences that, together with development and environmental factors, help shape risk.
Or to put it even more simply: genetic research has not identified a single defect. Instead, it has found many very small differences spread across the entire genome. Many genetic variants each contribute a tiny fraction to the risk—many of these overlap with other psychiatric diagnoses. A missing molecule, a dysfunctional receptor or a single cause does not feature in this picture.
Another important finding must be explicitly mentioned. The 2023 study found a clear link between ADHD-associated genes and genes that are active in dopaminergic midbrain neurons. Dopaminergic circuits are therefore involved.
The frequently cited twin heritability of ADHD is around 0.74, whilst the SNP heritability in the large-scale study was 0.14. This figure does not imply that ADHD is ‘74 or 14 per cent heritable’. It merely describes the proportion of the variation in the population studied that can be explained by the common, small genetic variants that such studies measure in the first place.
Common variants recorded in such studies can therefore only account for part of the differences.
The dopamine transporter
For a long time, imaging seemed to provide compelling evidence. In 2009, Nora Volkow and colleagues used positron emission tomography to study 53 adults with ADHD who were not receiving medication, as well as 44 adults without ADHD. In the nucleus accumbens – a brain region involved in motivation, reward anticipation and learning from feedback – the researchers found lower values than in the control group.
A meta-analysis by Fusar-Poli and colleagues in 2012 summarised nine SPECT and PET studies involving 169 people with ADHD and 173 controls. On average, the density of the dopamine transporter in a brain region (the striatum) was 14 per cent higher in those with ADHD. However, studies varied considerably.
This variation is revealing. The higher the proportion of participants who had never previously taken stimulants, the lower the transporter density. Previous treatment with stimulants could therefore explain a significant proportion of the conflicting results.
Consequently, transporter density is not a stable, unambiguous marker of the disorder. What was interpreted as a characteristic of ADHD may, at least in part, be attributable to the participant’s treatment history.
Medication does not prove a cause.
It is tempting to jump to conclusions. Stimulants increase the extracellular dopamine levels. They help many people with ADHD. Therefore, ADHD must be caused by a lack of dopamine.
François Gonon thoroughly debunked this conclusion in 2009. The effect of a medicine does not imply the cause of the symptoms it alleviates. Aspirin reduces fever. Fever is therefore not a result of a lack of aspirin.
The same applies to stimulants. Their efficacy in treating ADHD is well documented. Their effects relate to dopaminergic and noradrenergic processes. This provides a therapeutic target. It says nothing about the causes.
In 1978, Judith Rapoport and colleagues administered dextroamphetamine to fourteen healthy prepubertal boys in a double-blind study. Motor activity decreased, reaction times shortened, and performance on cognitive tests improved. The authors concluded that this cast doubt on the assumption that the indisputable response to stimulants in ADHD is unequivocally a characteristic of ADHD.
In 2015, Ilieva, Hook and Farah analysed 48 studies involving 1,409 people without ADHD. They found small but statistically significant effects on impulse control and short-term memory. After adjusting for publication bias, these effects were even smaller. Stimulants can also alter attention, alertness and motivation in people without ADHD. Their effects are therefore neither a diagnostic test nor evidence of a specific dopamine deficiency.
What the consensus paper says
The 2021 international consensus paper by the World Federation of ADHD, led by Stephen Faraone and authored by eighty contributors from 27 countries, brings together 208 evidence-based statements on ADHD. It does not contain any statement claiming that a dopamine deficiency causes ADHD.
Regarding the cause, it states that ADHD is rarely caused by a single genetic or environmental risk factor. Most cases arise from the interaction of many genetic and environmental influences, each contributing only a small amount.
Regarding imaging studies, it states that they reveal minor differences in brain structure and function but are not suitable for diagnosis. As for candidate genes such as DAT1 and DRD4, it states that their status as risk genes remains uncertain until confirmed by genome-wide studies.
In the authoritative consensus and genomic studies, therefore, dopamine deficiency does not appear to be the sole explanation.
How a shorthand formula endures
The parallel case of serotonin in depression illustrates a similar communicative mechanism. A simplified neurochemical explanation can continue to have an impact even after it is no longer presented in the specialist literature as a complete causal model. Above all, the comparison shows just how resilient biological shorthand is in the face of scientific progress.
Researchers have investigated how this persistence arises in the field of ADHD. In 2011, Gonon, Bezard and Boraud evaluated media coverage of ADHD research. Of 159 specialist articles claiming a link between DRD4 variants and ADHD, only 25 mentioned in their abstracts that the risk involved was low. Of 61 media articles covering two scientific papers, only one described the findings accurately.
This pattern continues on social media platforms. In 2022, Yeung, Ng and Abi-Jaoude examined the hundred most-viewed TikTok videos on ADHD: 52 per cent were misleading, 27 per cent were personal accounts, and 21 per cent were useful. The study focused on the quality of ADHD content in general, not specifically on the claim of a dopamine deficiency. However, it illustrates the context in which simplistic neurochemical narratives are effective.
And there is nothing wrong with simplicity, as long as facts are not distorted. A catchy explanation fosters understanding and provides guidance. Not everyone affected needs to delve into the research literature to manage their patterns successfully. The ‘dopamine deficiency’ concept can certainly serve this purpose. To return to the aspirin example: one needs to know that aspirin reduces a fever, and how much of it one can take safely when one has a fever. The treating doctor also needs to know what COX enzymes are and what function they serve.
What remains
What remains is a highly heritable, heterogeneous and developmentally related variety of causes. Many genetic variants contribute small risks that are not specific to ADHD. Environmental factors and development interact with them. Studies identify statistical differences in brain structure, brain function, reward processing and executive functions. These are clear-cut, but not useful for diagnosing individuals.
Dopaminergic and noradrenergic processes form part of this model, as do the experiences of those affected. And medication can be effective without compensating for a pre-existing biochemical deficit.
The ‘empty tank’ narrative is a good one, but it is incomplete
Key points in brief
• Dopamine is relevant to ADHD, but a uniform dopamine deficiency is not a sufficiently substantiated explanation.
• Large-scale genomic studies reveal a complex, polygenic and developmentally determined architecture. Nothing remains of the notion of a few ‘dopamine genes’.
• The 2023 study found an enrichment of ADHD-associated genes in dopaminergic midbrain neurons. This indicates the involvement of dopaminergic circuits. It says nothing about a deficiency.
• The findings regarding the dopamine transporter are contradictory and appear to be influenced, amongst other things, by prior stimulant treatment.
• Stimulants affect, amongst other things, dopaminergic and noradrenergic processes. However, their efficacy does not prove that a neurotransmitter deficiency causes ADHD.
• Major consensus studies describe ADHD as the result of many small genetic and environmental influences. None of these studies mentions a single biochemical deficit.
• The notion of a dopamine deficiency persists because it is easy to understand, offers reassurance and has commercial appeal. It has little to do with the current state of research.
Sources
· Demontis, D. et al.: Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder, Nature Genetics 51 (2019), 63–75: https://www.nature.com/articles/s41588-018-0269-7
· Demontis, D. et al.: Genome-wide analyses of ADHD identify 27 risk loci, refine the genetic architecture and implicate several cognitive domains, Nature Genetics 55 (2023), 198–208: https://www.nature.com/articles/s41588-022-01285-8
· Gizer, I. R., Ficks, C., Waldman, I. D.: Candidate gene studies of ADHD. A meta-analytic review, Human Genetics 126 (2009), 51–90: https://doi.org/10.1007/s00439-009-0694-x
· Grünblatt, E. et al.: Association study and a systematic meta-analysis of the DAT1/SLC6A3 3′‑UTR VNTR polymorphism in ADHD, Journal of Neural Transmission 126 (2019), 517–529: https://doi.org/10.1007/s00702-019-01998-x
· Bonvicini, C. et al.: DRD4 48 bp multiallelic variants as age- and population-specific biomarkers in ADHD, Translational Psychiatry 10 (2020), 70: https://doi.org/10.1038/s41398-020-0755-4
· Border, R. et al.: No support for historical candidate gene or candidate gene-by-interaction hypotheses for major depression across multiple large samples, American Journal of Psychiatry 176 (2019), 376–387: https://doi.org/10.1176/appi.ajp.2018.18070881
· Volkow, N. D. et al.: Evaluating the dopamine reward pathway in ADHD. Clinical implications, JAMA 302 (2009), 1084–1091: https://doi.org/10.1001/jama.2009.1308
· Fusar-Poli, P. et al.: Striatal dopamine transporter alterations in ADHD. Pathophysiology or adaptation to psychostimulants? A meta-analysis, American Journal of Psychiatry 169 (2012), 264–272: https://doi.org/10.1176/appi.ajp.2011.11060940
· Gonon, F.: The dopaminergic hypothesis of attention-deficit/hyperactivity disorder needs re-examining, Trends in Neurosciences 32 (2009), 2–8: https://doi.org/10.1016/j.tins.2008.09.010
· Moncrieff, J., Cohen, D.: Rethinking models of psychotropic drug action, Psychotherapy and Psychosomatics 74 (2005), 145–153: https://doi.org/10.1159/000083999
· Rapoport, J. L. et al.: Dextroamphetamine. Cognitive and behavioural effects in normal prepubertal boys, Science 199 (1978), 560–563: https://doi.org/10.1126/science.341313
· Ilieva, I. P., Hook, C. J., Farah, M. J.: Prescription Stimulants’ Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory. A Meta-analysis, Journal of Cognitive Neuroscience 27 (2015), 1069–1089: https://doi.org/10.1162/jocn_a_00776
· Faraone, S. V. et al.: The World Federation of ADHD International Consensus Statement. 208 Evidence-based conclusions about the disorder, *Neuroscience & Biobehavioural Reviews* 128 (2021), 789–818: https://pmc.ncbi.nlm.nih.gov/articles/PMC8328933/
· Moncrieff, J. et al.: The serotonin theory of depression. A systematic umbrella review of the evidence, Molecular Psychiatry 28 (2023), 3243–3256: https://doi.org/10.1038/s41380-022-01661-0
· Gonon, F., Bezard, E., Boraud, T.: Misrepresentation of neuroscience data might give rise to misleading conclusions in the media. The case of attention deficit hyperactivity disorder, PLoS ONE 6 (2011), e14618: https://doi.org/10.1371/journal.pone.0014618
· Yeung, A., Ng, E., Abi-Jaoude, E.: TikTok and Attention-Deficit/Hyperactivity Disorder. A Cross-Sectional Study of Social Media Content Quality, Canadian Journal of Psychiatry 67 (2022), 899–906: https://doi.org/10.1177/07067437221082854
Related
DESCRIPTION: The narrative of dopamine deficiency explains ADHD in a single sentence and has persisted for thirty years. What the major genome studies really show, and why the dopamine hypothesis has gaps.
ADHD and dopamine: Why a dopamine deficiency is not a sufficient explanation
The most common explanation for ADHD is: too little dopamine. It features in information leaflets, apps and millions of short videos. There is too little of this neurotransmitter in the ADHD brain; this is why there is a lack of drive, why people seek out stimuli, and why stimulants work, as they compensate for the deficiency.
However, large-scale genomic studies in recent years show that dopamine deficiency is not the sole cause of these behavioural and experiential patterns. Imaging studies provide even more contradictory results. The international consensus paper by experts does not describe ADHD as the result of such a deficiency. It is a model that aids understanding; it does not provide a complete explanation.
The image of an empty tank
This explanation has one obvious advantage: it fits into a single image. An empty tank. Too little fuel, too little drive, too much searching for the next stimulus. Medication fills the tank.
For many of those affected, this image serves a purpose:
· In practice, it offers a straightforward answer to a question that cannot otherwise be answered in five minutes.
· It takes the pressure off those affected by removing difficulties from the realm of moral judgement, such as lack of willpower, laziness, or character flaws.
· ‘Dopamine management’ helps with many problems associated with ADHD.
· But it also lends itself to digital self-optimisation, dietary supplements and focus-enhancing products, as it provides an intuitive problem-solving framework.
Where the idea came from
Researchers investigated whether certain variants of two genes occur slightly more frequently in ADHD. Both genes are associated with the dopamine system. However, the results were weak and inconsistent. Nevertheless, they gave rise to a plausible hypothesis: if dopamine plays a role in ADHD, variants in genes of the dopaminergic system could increase the risk.
At the time, meta-analyses identified isolated statistical associations. The 2009 meta-analysis by Gizer, Ficks and Waldman reported associations for DAT1, DRD4, DRD5 and other genes, whilst also noting considerable differences between the studies. Later and larger analyses showed significantly smaller effects.
In the case of a variant of the dopamine transporter gene DAT1, Grünblatt and colleagues found a very small statistical association with ADHD in children and adolescents. An odds ratio of 1.105 means that the variant was only slightly more common in those affected – not, for example, ‘ten per cent more ADHD’ and certainly not an indication of a causal link. This association was not observed in adults.
For a variant of the dopamine receptor gene DRD4, Bonvicini and colleagues found an association only in a specific group: children of European descent. Furthermore, they did not examine the same genetic loci as those investigated in the large, more recent genome-wide studies. Those studies found no association.
In short: individual variants in dopamine genes may be marginally associated with ADHD in some studies. However, they do not explain ADHD – and the results are too weak and too inconsistent to allow us to derive a simple narrative about the ‘dopamine gene’ or ‘dopamine deficiency’. Dopamine still plays a role in ADHD research. But the initial assumption that a few ‘dopamine genes’ explained ADHD did not stand up to scrutiny in larger sample sizes.
What the large-scale studies show
In 2019, researchers analysed the genetic data of more than 55,000 people – both with and without ADHD. They were not looking for a single ‘ADHD gene’, but rather for many small genetic differences that occur slightly more frequently in people with ADHD. In doing so, they identified 12 genetic loci statistically associated with ADHD.
In 2023, the researchers repeated the study with a much larger group: more than 225,000 people. This time, the researchers identified 27 such genetic loci and 76 genes that may be involved. Many of these genes are primarily active during the very early stages of brain development, including in areas of the frontal lobe important for planning, attention, and impulse control.
The key finding is this: ADHD cannot be attributed to a single gene, a specific area of the brain or a neurotransmitter such as dopamine. Rather, it involves many small genetic influences that, together with development and environmental factors, help shape risk.
Or to put it even more simply: genetic research has not identified a single defect. Instead, it has found many very small differences spread across the entire genome. Many genetic variants each contribute a tiny fraction to the risk—many of these overlap with other psychiatric diagnoses. A missing molecule, a dysfunctional receptor or a single cause does not feature in this picture.
Another important finding must be explicitly mentioned. The 2023 study found a clear link between ADHD-associated genes and genes that are active in dopaminergic midbrain neurons. Dopaminergic circuits are therefore involved.
The frequently cited twin heritability of ADHD is around 0.74, whilst the SNP heritability in the large-scale study was 0.14. This figure does not imply that ADHD is ‘74 or 14 per cent heritable’. It merely describes the proportion of the variation in the population studied that can be explained by the common, small genetic variants that such studies measure in the first place.
Common variants recorded in such studies can therefore only account for part of the differences.
The dopamine transporter
For a long time, imaging seemed to provide compelling evidence. In 2009, Nora Volkow and colleagues used positron emission tomography to study 53 adults with ADHD who were not receiving medication, as well as 44 adults without ADHD. In the nucleus accumbens – a brain region involved in motivation, reward anticipation and learning from feedback – the researchers found lower values than in the control group.
A meta-analysis by Fusar-Poli and colleagues in 2012 summarised nine SPECT and PET studies involving 169 people with ADHD and 173 controls. On average, the density of the dopamine transporter in a brain region (the striatum) was 14 per cent higher in those with ADHD. However, studies varied considerably.
This variation is revealing. The higher the proportion of participants who had never previously taken stimulants, the lower the transporter density. Previous treatment with stimulants could therefore explain a significant proportion of the conflicting results.
Consequently, transporter density is not a stable, unambiguous marker of the disorder. What was interpreted as a characteristic of ADHD may, at least in part, be attributable to the participant’s treatment history.
Medication does not prove a cause.
It is tempting to jump to conclusions. Stimulants increase the extracellular dopamine levels. They help many people with ADHD. Therefore, ADHD must be caused by a lack of dopamine.
François Gonon thoroughly debunked this conclusion in 2009. The effect of a medicine does not imply the cause of the symptoms it alleviates. Aspirin reduces fever. Fever is therefore not a result of a lack of aspirin.
The same applies to stimulants. Their efficacy in treating ADHD is well documented. Their effects relate to dopaminergic and noradrenergic processes. This provides a therapeutic target. It says nothing about the causes.
In 1978, Judith Rapoport and colleagues administered dextroamphetamine to fourteen healthy prepubertal boys in a double-blind study. Motor activity decreased, reaction times shortened, and performance on cognitive tests improved. The authors concluded that this cast doubt on the assumption that the indisputable response to stimulants in ADHD is unequivocally a characteristic of ADHD.
In 2015, Ilieva, Hook and Farah analysed 48 studies involving 1,409 people without ADHD. They found small but statistically significant effects on impulse control and short-term memory. After adjusting for publication bias, these effects were even smaller. Stimulants can also alter attention, alertness and motivation in people without ADHD. Their effects are therefore neither a diagnostic test nor evidence of a specific dopamine deficiency.
What the consensus paper says
The 2021 international consensus paper by the World Federation of ADHD, led by Stephen Faraone and authored by eighty contributors from 27 countries, brings together 208 evidence-based statements on ADHD. It does not contain any statement claiming that a dopamine deficiency causes ADHD.
Regarding the cause, it states that ADHD is rarely caused by a single genetic or environmental risk factor. Most cases arise from the interaction of many genetic and environmental influences, each contributing only a small amount.
Regarding imaging studies, it states that they reveal minor differences in brain structure and function but are not suitable for diagnosis. As for candidate genes such as DAT1 and DRD4, it states that their status as risk genes remains uncertain until confirmed by genome-wide studies.
In the authoritative consensus and genomic studies, therefore, dopamine deficiency does not appear to be the sole explanation.
How a shorthand formula endures
The parallel case of serotonin in depression illustrates a similar communicative mechanism. A simplified neurochemical explanation can continue to have an impact even after it is no longer presented in the specialist literature as a complete causal model. Above all, the comparison shows just how resilient biological shorthand is in the face of scientific progress.
Researchers have investigated how this persistence arises in the field of ADHD. In 2011, Gonon, Bezard and Boraud evaluated media coverage of ADHD research. Of 159 specialist articles claiming a link between DRD4 variants and ADHD, only 25 mentioned in their abstracts that the risk involved was low. Of 61 media articles covering two scientific papers, only one described the findings accurately.
This pattern continues on social media platforms. In 2022, Yeung, Ng and Abi-Jaoude examined the hundred most-viewed TikTok videos on ADHD: 52 per cent were misleading, 27 per cent were personal accounts, and 21 per cent were useful. The study focused on the quality of ADHD content in general, not specifically on the claim of a dopamine deficiency. However, it illustrates the context in which simplistic neurochemical narratives are effective.
And there is nothing wrong with simplicity, as long as facts are not distorted. A catchy explanation fosters understanding and provides guidance. Not everyone affected needs to delve into the research literature to manage their patterns successfully. The ‘dopamine deficiency’ concept can certainly serve this purpose. To return to the aspirin example: one needs to know that aspirin reduces a fever, and how much of it one can take safely when one has a fever. The treating doctor also needs to know what COX enzymes are and what function they serve.
What remains
What remains is a highly heritable, heterogeneous and developmentally related variety of causes. Many genetic variants contribute small risks that are not specific to ADHD. Environmental factors and development interact with them. Studies identify statistical differences in brain structure, brain function, reward processing and executive functions. These are clear-cut, but not useful for diagnosing individuals.
Dopaminergic and noradrenergic processes form part of this model, as do the experiences of those affected. And medication can be effective without compensating for a pre-existing biochemical deficit.
The ‘empty tank’ narrative is a good one, but it is incomplete
Key points in brief
• Dopamine is relevant to ADHD, but a uniform dopamine deficiency is not a sufficiently substantiated explanation.
• Large-scale genomic studies reveal a complex, polygenic and developmentally determined architecture. Nothing remains of the notion of a few ‘dopamine genes’.
• The 2023 study found an enrichment of ADHD-associated genes in dopaminergic midbrain neurons. This indicates the involvement of dopaminergic circuits. It says nothing about a deficiency.
• The findings regarding the dopamine transporter are contradictory and appear to be influenced, amongst other things, by prior stimulant treatment.
• Stimulants affect, amongst other things, dopaminergic and noradrenergic processes. However, their efficacy does not prove that a neurotransmitter deficiency causes ADHD.
• Major consensus studies describe ADHD as the result of many small genetic and environmental influences. None of these studies mentions a single biochemical deficit.
• The notion of a dopamine deficiency persists because it is easy to understand, offers reassurance and has commercial appeal. It has little to do with the current state of research.
Sources
· Demontis, D. et al.: Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder, Nature Genetics 51 (2019), 63–75: https://www.nature.com/articles/s41588-018-0269-7
· Demontis, D. et al.: Genome-wide analyses of ADHD identify 27 risk loci, refine the genetic architecture and implicate several cognitive domains, Nature Genetics 55 (2023), 198–208: https://www.nature.com/articles/s41588-022-01285-8
· Gizer, I. R., Ficks, C., Waldman, I. D.: Candidate gene studies of ADHD. A meta-analytic review, Human Genetics 126 (2009), 51–90: https://doi.org/10.1007/s00439-009-0694-x
· Grünblatt, E. et al.: Association study and a systematic meta-analysis of the DAT1/SLC6A3 3′‑UTR VNTR polymorphism in ADHD, Journal of Neural Transmission 126 (2019), 517–529: https://doi.org/10.1007/s00702-019-01998-x
· Bonvicini, C. et al.: DRD4 48 bp multiallelic variants as age- and population-specific biomarkers in ADHD, Translational Psychiatry 10 (2020), 70: https://doi.org/10.1038/s41398-020-0755-4
· Border, R. et al.: No support for historical candidate gene or candidate gene-by-interaction hypotheses for major depression across multiple large samples, American Journal of Psychiatry 176 (2019), 376–387: https://doi.org/10.1176/appi.ajp.2018.18070881
· Volkow, N. D. et al.: Evaluating the dopamine reward pathway in ADHD. Clinical implications, JAMA 302 (2009), 1084–1091: https://doi.org/10.1001/jama.2009.1308
· Fusar-Poli, P. et al.: Striatal dopamine transporter alterations in ADHD. Pathophysiology or adaptation to psychostimulants? A meta-analysis, American Journal of Psychiatry 169 (2012), 264–272: https://doi.org/10.1176/appi.ajp.2011.11060940
· Gonon, F.: The dopaminergic hypothesis of attention-deficit/hyperactivity disorder needs re-examining, Trends in Neurosciences 32 (2009), 2–8: https://doi.org/10.1016/j.tins.2008.09.010
· Moncrieff, J., Cohen, D.: Rethinking models of psychotropic drug action, Psychotherapy and Psychosomatics 74 (2005), 145–153: https://doi.org/10.1159/000083999
· Rapoport, J. L. et al.: Dextroamphetamine. Cognitive and behavioural effects in normal prepubertal boys, Science 199 (1978), 560–563: https://doi.org/10.1126/science.341313
· Ilieva, I. P., Hook, C. J., Farah, M. J.: Prescription Stimulants’ Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory. A Meta-analysis, Journal of Cognitive Neuroscience 27 (2015), 1069–1089: https://doi.org/10.1162/jocn_a_00776
· Faraone, S. V. et al.: The World Federation of ADHD International Consensus Statement. 208 Evidence-based conclusions about the disorder, *Neuroscience & Biobehavioural Reviews* 128 (2021), 789–818: https://pmc.ncbi.nlm.nih.gov/articles/PMC8328933/
· Moncrieff, J. et al.: The serotonin theory of depression. A systematic umbrella review of the evidence, Molecular Psychiatry 28 (2023), 3243–3256: https://doi.org/10.1038/s41380-022-01661-0
· Gonon, F., Bezard, E., Boraud, T.: Misrepresentation of neuroscience data might give rise to misleading conclusions in the media. The case of attention deficit hyperactivity disorder, PLoS ONE 6 (2011), e14618: https://doi.org/10.1371/journal.pone.0014618
· Yeung, A., Ng, E., Abi-Jaoude, E.: TikTok and Attention-Deficit/Hyperactivity Disorder. A Cross-Sectional Study of Social Media Content Quality, Canadian Journal of Psychiatry 67 (2022), 899–906: https://doi.org/10.1177/07067437221082854
Related
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Möchten Sie informiert werden, wenn ich einen neuen Blogbeitrag veröffentliche? Tragen Sie sich gern hier ein.
Klicken Sie auf „Kostenlos abonnieren“, wenn Sie meine Datenschutzerklärung gelesen und akzeptiert haben. Ihre Einwilligung können Sie jederzeit widerrufen.