<p>I hope the few sources below answer your question. <strong>I strongly recommend you read actual sources as opposed to the parts I have quoted.</strong> I don't know much about this topic so I did not attempt to translate anything in laymen terms, since I might have distorted or misinterpreted information in the process. However, the three sources below are one of the best-known studies on the genetic basis of ADHD. I have quoted the two sources in direct response to your question about the proposed role of dopamine and serotonin transporter genes.</p>

<p><strong>Percentage due to variation attributed to heritability</strong> </p>

<blockquote>
  <p>Twin, family and adoption studies have suggested that there is a strong genetic contribution to ADHD, with a mean heritability estimate of 76 % However, it has been difficult to implicate any specific gene in ADHD beyond reasonable doubt. The difficulties encountered in identifying genetic variants increasing the risk for ADHD could be at least in part owing to the heterogeneity and complexity of this clinical syndrome.Consequently, it has been proposed that the use of intermediate phenotypes (or endophenotypes) relevant to ADHD are likely to be more informative than the DSM-IV1 diagnoses, allowing for increased detection of genetic effects.</p>
</blockquote>

<p><strong>Genome-wide linkage scans</strong></p>

<blockquote>
  <p>To date, seven genome-wide ADHD linkage scans have been published and
  some chromosome regions such as 5p13, 14q12, and 17p11 have been
  indicated in multiple studies [Fisher et al., 2002; Bakker et al.,
  2003; Arcos-Burgos et al., 2004; Hebebrand et al., 2006; Ogdie et al.,
  2006; Faraone et al., 2007; Asherson et al., 2008; Romanos et al.,
  2008]. However, no chromosome region has been consistently identified
  across the scans and the majority of the findings were unique to each
  study. This is not unexpected because the power of individual scans is
  likely to be low for a complex trait such as ADHD which may only have
  genes of small to moderate effects [Risch and Merikangas, 1996;
  Waldman and Gizer, 2006].</p>
</blockquote>

<p><strong>Dopamine transporter (DAT1)</strong></p>

<blockquote>
  <p>The DA transporter (DAT1) gene harbours a 40-bp repeat sequence
  variable number tandem repeat polymorphism located in the
  3′-untranslated region. The most common alleles are the 10- (480-bp,
  71.9%) and 9-repeat (440-bp, 23.4%) alleles, although these frequencies are variable from one population to the next.
  Homozygosity for the 10-repeat allele was reported to be associated
  with higher DA transporter protein in the striatum, a region
  where it is heavily expressed56 and where it serves as the primary
  means of DA reuptake. Several studies have suggested a relation
  between ADHD and the DAT1 variable number tandem repeat, the 10-repeat
  allele being the risk allele; however, a roughly equal number of
  studies have failed to detect such a relation. In a review by Faraone
  and colleagues, the pooled OR associated with the 10-repeat allele in
  family-based association studies was estimated to be 1.13 (95% CI
  1.03–1.24).</p>
  
  <p>Loo and colleagues40 reported that children carrying 2 copies of the
  10-repeat allele exhibit higher commission errors, impulsive responses
  (β score) and reaction time variability compared with carriers of the
  9-repeat allele. Bellgrove and colleagues, who used a CPT–like task
  (the sustained attention to response task), found higher reaction time
  variability in children who were homozygous for the 10-repeat allele.
  However, in this study, the 2 groups did not differ in omission and
  commission errors.</p>
</blockquote>

<p><strong>Trypotphan hydroxylase 2 (TPH2)</strong></p>

<blockquote>
  <p>The TPH2 gene encodes the rate-limiting enzyme in the synthesis of
  serotonin in humans and was shown to be associated with completed
  suicide and major depression. Four studies have shown an
  association between multiple SNPs in this gene and ADHD.
  Recently, a significant association was observed between total errors
  of omission in the test of variables of attention and 2 SNPs
  (rs1386488, rs6582072). Similarly, a significant association was
  observed between rs1386488 and another SNP (rs1386497) and total
  reaction time scores as well as total reaction time variability
  scores. These intronic SNPs are part of 8 markers found to have strong
  linkage disequilibrium with each other and that compose a single
  haplotype block associated with ADHD in the tested sample. A second
  study tested IQ level and 4 SNPs previously reported to be associated
  with ADHD, but analyses were negative.</p>
</blockquote>

<hr>

<p><strong>Sources:</strong></p>

<p><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647566/" rel="nofollow">Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies.</a> <br>
Oussama Kebir, Karim Tabbane, Sarojini Sengupta, Ridha Joober <br>
<em>J Psychiatry Neurosci.</em> March 2009; 34(2): 88–101.</p>

<p><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847260/" rel="nofollow">Molecular Genetics of Attention Deficit Hyperactivity Disorder</a> <br>
Stephen V. Faraone, Eric Mick <br>
<em>Psychiatr Clin North Am.</em> 2010 March; 33(1): 159–180.</p>

<p><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890047/" rel="nofollow">Meta-Analysis of Genome-Wide Linkage Scans of Attention Deficit Hyperactivity Disorder</a> <br>
Karin Zhou et. al. <br>
<em>Am J Med Genet B Neuropsychiatr Genet.</em> 5th December 2008; 147B(8): 1392–1398.</p>

CC BY-SA 3.0
2015-10-09T19:48:03.543Z
2015-10-09T19:48:03.543Z
Vakalate
<p>According to <a href="http://psychcentral.com/news/2013/08/19/5-major-mental-illnesses-traced-to-same-genetic-variations/58642.html" rel="nofollow noreferrer">Psychcentral</a> depression, bipolar disorder, ADHD, schizophrenia and autism are traceable to the same inherited genetic variations</p>

<p>According to <a href="https://youtu.be/GOK1tKFFIQI?t=98" rel="nofollow noreferrer">AsapSCIENCE</a>, depression could be genetic due to a variation in the serotonin transporter gene. Having at least one short seems to give some kind of genetic predisposition to depression.</p>

<p>So what's the analogue of the serotonin transporter gene in ADHD? Is there a dopamine transporter gene?</p>

<p>I have <a href="https://biology.stackexchange.com/questions/38716/in-what-way-is-adhd-genetic">double posted</a> this question on the Biology StackExchange.</p>

<abnormal-psychology><adhd><genetics>
What is the underlying genetic basis for ADHD?
BCLC
# What is the underlying genetic basis for ADHD?

(Asked by: username_0 on 2015-10-05)

According to [Psychcentral](http://psychcentral.com/news/2013/08/19/5-major-mental-illnesses-traced-to-same-genetic-variations/58642.html) depression, bipolar disorder, ADHD, schizophrenia and autism are traceable to the same inherited genetic variations

According to [AsapSCIENCE](https://youtu.be/GOK1tKFFIQI?t=98), depression could be genetic due to a variation in the serotonin transporter gene. Having at least one short seems to give some kind of genetic predisposition to depression.

So what's the analogue of the serotonin transporter gene in ADHD? Is there a dopamine transporter gene?

I have [double posted](https://biology.stackexchange.com/questions/38716/in-what-way-is-adhd-genetic) this question on the Biology StackExchange.

**Tags:** abnormal-psychology, adhd, genetics


---

## 1 answers

### Answer by username_1 on 2015-10-09. Score: 3 | Accepted answer

I hope the few sources below answer your question. **I strongly recommend you read actual sources as opposed to the parts I have quoted.** I don't know much about this topic so I did not attempt to translate anything in laymen terms, since I might have distorted or misinterpreted information in the process. However, the three sources below are one of the best-known studies on the genetic basis of ADHD. I have quoted the two sources in direct response to your question about the proposed role of dopamine and serotonin transporter genes.

**Percentage due to variation attributed to heritability**

> Twin, family and adoption studies have suggested that there is a strong genetic contribution to ADHD, with a mean heritability estimate of 76 % However, it has been difficult to implicate any specific gene in ADHD beyond reasonable doubt. The difficulties encountered in identifying genetic variants increasing the risk for ADHD could be at least in part owing to the heterogeneity and complexity of this clinical syndrome.Consequently, it has been proposed that the use of intermediate phenotypes (or endophenotypes) relevant to ADHD are likely to be more informative than the DSM-IV1 diagnoses, allowing for increased detection of genetic effects.

**Genome-wide linkage scans**

> To date, seven genome-wide ADHD linkage scans have been published and
> some chromosome regions such as 5p13, 14q12, and 17p11 have been
> indicated in multiple studies [Fisher et al., 2002; Bakker et al.,
> 2003; Arcos-Burgos et al., 2004; Hebebrand et al., 2006; Ogdie et al.,
> 2006; Faraone et al., 2007; Asherson et al., 2008; Romanos et al.,
> 2008]. However, no chromosome region has been consistently identified
> across the scans and the majority of the findings were unique to each
> study. This is not unexpected because the power of individual scans is
> likely to be low for a complex trait such as ADHD which may only have
> genes of small to moderate effects [Risch and Merikangas, 1996;
> Waldman and Gizer, 2006].

**Dopamine transporter (DAT1)**

> The DA transporter (DAT1) gene harbours a 40-bp repeat sequence
> variable number tandem repeat polymorphism located in the
> 3′-untranslated region. The most common alleles are the 10- (480-bp,
> 71.9%) and 9-repeat (440-bp, 23.4%) alleles, although these frequencies are variable from one population to the next.
> Homozygosity for the 10-repeat allele was reported to be associated
> with higher DA transporter protein in the striatum, a region
> where it is heavily expressed56 and where it serves as the primary
> means of DA reuptake. Several studies have suggested a relation
> between ADHD and the DAT1 variable number tandem repeat, the 10-repeat
> allele being the risk allele; however, a roughly equal number of
> studies have failed to detect such a relation. In a review by Faraone
> and colleagues, the pooled OR associated with the 10-repeat allele in
> family-based association studies was estimated to be 1.13 (95% CI
> 1.03–1.24).
>
> Loo and colleagues40 reported that children carrying 2 copies of the
> 10-repeat allele exhibit higher commission errors, impulsive responses
> (β score) and reaction time variability compared with carriers of the
> 9-repeat allele. Bellgrove and colleagues, who used a CPT–like task
> (the sustained attention to response task), found higher reaction time
> variability in children who were homozygous for the 10-repeat allele.
> However, in this study, the 2 groups did not differ in omission and
> commission errors.

**Trypotphan hydroxylase 2 (TPH2)**

> The TPH2 gene encodes the rate-limiting enzyme in the synthesis of
> serotonin in humans and was shown to be associated with completed
> suicide and major depression. Four studies have shown an
> association between multiple SNPs in this gene and ADHD.
> Recently, a significant association was observed between total errors
> of omission in the test of variables of attention and 2 SNPs
> (rs1386488, rs6582072). Similarly, a significant association was
> observed between rs1386488 and another SNP (rs1386497) and total
> reaction time scores as well as total reaction time variability
> scores. These intronic SNPs are part of 8 markers found to have strong
> linkage disequilibrium with each other and that compose a single
> haplotype block associated with ADHD in the tested sample. A second
> study tested IQ level and 4 SNPs previously reported to be associated
> with ADHD, but analyses were negative.

---

**Sources:**

[Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies.](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647566/)   
Oussama Kebir, Karim Tabbane, Sarojini Sengupta, Ridha Joober   
*J Psychiatry Neurosci.* March 2009; 34(2): 88–101.

[Molecular Genetics of Attention Deficit Hyperactivity Disorder](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847260/)   
Stephen V. Faraone, Eric Mick   
*Psychiatr Clin North Am.* 2010 March; 33(1): 159–180.

[Meta-Analysis of Genome-Wide Linkage Scans of Attention Deficit Hyperactivity Disorder](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890047/)   
Karin Zhou et. al.   
*Am J Med Genet B Neuropsychiatr Genet.* 5th December 2008; 147B(8): 1392–1398.


---

