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.
Oussama Kebir, Karim Tabbane, Sarojini Sengupta, Ridha Joober
J Psychiatry Neurosci. March 2009; 34(2): 88–101.
Molecular Genetics of Attention Deficit Hyperactivity Disorder
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
Karin Zhou et. al.
Am J Med Genet B Neuropsychiatr Genet. 5th December 2008; 147B(8): 1392–1398.
