Molecular Genetics of Attention Deficit Hyperactivity Disorder

By Stephen V. Faraone, E. Mick. Psychiatric Clinics of North America, 2010

1,344 citations recorded by the source corpus.

Summary Although twin studies demonstrate that ADHD is a highly heritable condition, molecular genetic studies suggest that the genetic architecture of ADHD is complex. The handful of genome-wide linkage and association scans that have been conducted thus far show divergent findings and are, therefore, not conclusive. Similarly, many of the candidate genes reviewed here (i.e. DBH, MAOA, SLC6A2, TPH-2, SLC6A4, CHRNA4, GRIN2A) are theoretically compelling from neurobiological systems perspective but available data are sparse and inconsistent. However, candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder, with meta-analyses supportive of a role of the genes coding for DRD4, DRD5, SLC6A3, SNAP-25, and HTR1B in the etiology of ADHD.

Subfields: Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/bab592c5e9b6c9e885fda54dbea7fdd16a303927

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Citations in the corpus

Attention‐Deficit‐Hyperactivity Disorder: An Update (2009, background): “A review of studies in twins showed that about 75% of the variance in ADHD traits is attributable to genetics.(20) Although several studies have identified many different chromosomal regions associated with ADHD, there is often minimal overlap among studies in terms of specific genes indentified.”
European consensus statement on diagnosis and treatment of adult ADHD: The European Network Adult ADHD (2010, background): “Family, twin and adoption studies show that ADHD is a familial disorder with high heritability, indicating that a significant genetic component influences risk for the disorder [45-53].”
Practitioner Review: What have we learnt about the causes of ADHD? (2013, background): “First degree relatives of those with ADHD are two to eight times more likely than relatives of unaffected individuals to also show ADHD (Faraone et al., 2005).”
ASD and ADHD have a similar burden of rare protein-truncating variants (2018, neutral): “The remaining ASD (4,084), ADHD (3,536), ASD+ADHD (727), and control (5,214) samples were the ones used in this study.”
Drosophila strategies to study psychiatric disorders. (2013, background): “Many candidate genes have been described in recent years, which have led to the discovery of disease pathways involving dopamine and serotonin [16,53,54,127].”
ADHD-like behavior and entrepreneurial intentions (2013, background): “2014) with genetics contributing to about 60–75 % of cases (Cortese 2012; Faraone et al. 2005).”
The role of the posterior cingulate cortex in cognition and disease. (2014, background): “ADHD has a strong hereditary component, and a number of candidate genes have been identified (Faraone et al., 2005).”