There have been several investigative attempts at a molecular level to identify genes implicated in ADHD. Studies, for example, such as the GWAS (genome-wide association studies) and the IMAGE project (international multisite ADHD gene) have contributed towards large datasets which show an association of ADHD with 18 genes .
There are also several genetic variants within more than a few genes involved in the regulation of neurotransmitter systems (e.g., dopamine, norepinephrine and serotonin) which have been linked with an increased risk for ADHD [78, 79].
Some of these genetic variations are listed below:
- dopamine receptors 4  (DRD4 7-repeat allele) and 5  (DRD5 148bp-allele)
- dopamine beta-hydroxylase gene  (DBH, 5’ taq1 A allele)
- synapto-somal-associated protein 25 gene  (SNAP-25, T1065G single-nucleotide polymorphism SNP)
- serotonin transporter gene  (SLC6A4, 44-bp insertion/deletion in the promoter region (5-HTTLPR)
- serotonin 1B receptor gene  (HTR1B, G861C SNP)
Sub-microscopic structural chromosomal abnormalities, also known as copy number variants (CNVs), are a notable source of genetic variation [82, 83]. Large, rare CNVs are implicated in neurodevelopmental disorders including autism and schizophrenia [84-86]. New evidence has supported a role for a highly significant increase in the prevalence of CNVs existing in children with ADHD and those with intellectual delay compared to controls . However, although genetic influences are substantial, the chemical pathways involved are not yet fully worked out and further investigations in this field are necessary.