Review: Genetics of attention deficit/hyperactivity disorder.
OBJECTIVE
The intent of this review is to provide an overview for the practicing psychologist/psychiatrist regarding the complexities of and the most recent advances made in the study of the genetic basis of attention-deficit/hyperactivity disorder (ADHD).


METHODS
We review a variety of concepts including: (a) complexities involved in studying the genetics of ADHD, (b) evidence for a primarily genetic component of ADHD, (c) evidence suggesting that there are only a few genes with major effects contributing to ADHD, (d) identification of the best candidate genes, (e) linkage analysis for the identification of novel candidate genes, and (f) data on gene-environment interactions.


RESULTS
It is now generally accepted that ADHD has a biological and even primarily genetic basis. However, despite the identification of several candidate genes, none of them seems to have a substantial effect and the exact etiology underlying ADHD has remained elusive. Genome-wide linkage analysis can help in the identification of novel candidate genes. While several independent groups have initiated these studies, we await further details and specific genes from fine-mapping studies. Most recently, researchers have been trying to identify gene by environment interactions to help understand ADHD. Replication of positive findings will be essential in teasing out these combinatorial influences.


CONCLUSIONS
Ideally, one day specific genes with major effects and specific risk factors with which they interact will be identified and we will be able to implement personalized medicine. Knowledge of such genes will allow us to identify specific diagnostic biological markers. In addition, defining the target genes is the first step in developing novel drug therapies to treat the ADHD symptoms that lead to impairment. Furthermore, such markers could also identify at risk individuals at a younger age in order to implement treatments sooner to decrease the severity of ADHD symptoms or even to prevent future ADHD symptomatology.
Wallis
Deeann
D
Texas Institute for Genomic Medicine, 2121 W Holcombe Blvd., Houston, TX 77030, USA. dwallis@tigm.org
Russell
Heather F
HF
Muenke
Maximilian
M
D001289:Attention Deficit Disorder with Hyperactivity / Q000235:genetics* / Q000523:psychology; D002648:Child; D002874:Chromosome Mapping; D015897:Comorbidity; D004200:Diseases in Twins / Q000235:genetics; D050483:Dopamine Plasma Membrane Transport Proteins / Q000235:genetics; D044127:Epigenesis, Genetic / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006801:Humans; D001523:Mental Disorders / Q000235:genetics; D010375:Pedigree; D010641:Phenotype; D050638:Receptors, Dopamine D4 / Q000235:genetics; D012307:Risk Factors; D012931:Social Environment; D018433:Twin Studies as Topic
C493599:DRD4 protein, human; D050483:Dopamine Plasma Membrane Transport Proteins; C493214:SLC6A3 protein, human; D050638:Receptors, Dopamine D4