TY - JOUR
T1 - Attention-deficit/hyperactivity disorder genomics
T2 - Update for clinicians
AU - Elia, Josephine
AU - Sackett, Jillan
AU - Turner, Terri
AU - Schardt, Martin
AU - Tang, Shih Ching
AU - Kurtz, Nicole
AU - Dunfey, Maura
AU - McFarlane, Nadia A.
AU - Susi, Aita
AU - Danish, David
AU - Li, Alice
AU - Nissley-Tsiopinis, Jenelle
AU - Borgmann-Winter, Karin
PY - 2012/10
Y1 - 2012/10
N2 - Attention deficit, hyperactivity disorder (ADHD) is familial and highly heritable. Several candidate genes involved in neurotransmission have been identified, however these confer minimal risk, suggesting that for the most part, ADHD is not caused by single common genetic variants. Advances in genotyping enabling investigation at the level of the genome have led to the discovery of rare structural variants suggesting that ADHD is a genomic disorder, with potentially thousands of variants, and common neuronal pathways disrupted by numerous rare variants resulting in similar ADHD phenotypes. Heritability studies in humans also indicate the importance of epigenetic factors, and animal studies are deciphering some of the processes that confer risk during gestation and throughout the post-natal period. These and future discoveries will lead to improved diagnosis, individualized treatment, cures, and prevention. These advances also highlight ethical and legal issues requiring management and interpretation of genetic data and ensuring privacy and protection from misuse.
AB - Attention deficit, hyperactivity disorder (ADHD) is familial and highly heritable. Several candidate genes involved in neurotransmission have been identified, however these confer minimal risk, suggesting that for the most part, ADHD is not caused by single common genetic variants. Advances in genotyping enabling investigation at the level of the genome have led to the discovery of rare structural variants suggesting that ADHD is a genomic disorder, with potentially thousands of variants, and common neuronal pathways disrupted by numerous rare variants resulting in similar ADHD phenotypes. Heritability studies in humans also indicate the importance of epigenetic factors, and animal studies are deciphering some of the processes that confer risk during gestation and throughout the post-natal period. These and future discoveries will lead to improved diagnosis, individualized treatment, cures, and prevention. These advances also highlight ethical and legal issues requiring management and interpretation of genetic data and ensuring privacy and protection from misuse.
KW - ADHD
KW - ADHD comorbidity
KW - Attention-deficit/hyperactivity disorder
KW - Copy number variation
KW - Epigenetics
KW - Ethics/laws
KW - Genetics
KW - Pharmacogenetics
KW - Structural variants
UR - https://www.scopus.com/pages/publications/84870783570
U2 - 10.1007/s11920-012-0309-4
DO - 10.1007/s11920-012-0309-4
M3 - Article
C2 - 22843546
AN - SCOPUS:84870783570
SN - 1523-3812
VL - 14
SP - 579
EP - 589
JO - Current Psychiatry Reports
JF - Current Psychiatry Reports
IS - 5
ER -