Attention Deficit Hyperactivity Disorder: Insight from Quantitative Genetic Research

Author(s):  
Alexis C. Frazier-Wood ◽  
Anna S. Rommel ◽  
Jonna Kuntsi
1997 ◽  
Vol 42 (6) ◽  
pp. 569-576 ◽  
Author(s):  
Michael Rutter

Objective: To review implications of genetic research in child psychiatry. Method: Key advances in quantitative and molecular genetics are noted and findings are summarized with respect to autism, attention-deficit hyperactivity disorder, oppositional defiant and conduct disorders, depression, schizophrenia, and Tourette's syndrome. Conclusions: Genetic findings will be helpful clinically in the elucidation of disordered brain processes, the understanding of nature–nurture interplay, diagnosis, genetic counselling, and pharmacotherapy.


2004 ◽  
Vol 38 (1-2) ◽  
pp. 10-19
Author(s):  
Max Yeh ◽  
Katherine I. Morley ◽  
Wayne D. Hall

Objective To review the policy and ethical implications of recent research on the molecular genetics of attention deficit hyperactivity disorder (ADHD). Method MEDLINE and psyclNFO database searches were used to identify studies on the genetics of ADHD. The implications of replicated candidate genes are discussed. Results The findings for most genes have been inconsistent but several studies have implicated the genes in the dopaminergic pathway in the aetiology of ADHD. Conclusions The current evidence on the genetics of ADHD is insufficient to justify genetic screening tests but it will provide important clues as to the aetiology of ADHD. Genetic information on susceptibility to ADHD has the potential to be abused and to stigmatize individuals. Researchers and clinicians need to be mindful of these issues in interpreting and disseminating the results of genetic studies of ADHD. Key words: ADHD, ethics, genetics, policy implications.


CNS Spectrums ◽  
1999 ◽  
Vol 4 (5) ◽  
pp. 49-52 ◽  
Author(s):  
Ranga Ram ◽  
Kim M. Schindler ◽  
Amy Bauer ◽  
Carlos N. Pato ◽  
Michele T. Pato

AbstractAttention-deficit/hyperactivity disorder (ADHD) has an early childhood onset in the majority of cases. This has a considerable impact on the development of the affected individual, both directly (as a result of the symptoms) and indirectly (through the stresses imposed upon school, learning, socialization, and family life). Several lines of evidence point to a genetic component to ADHD. Family studies show a familial aggregation of ADHD, with a five- to sixfold increase in the incidence of ADHD among first-degree relatives. Twin studies reveal a higher concordance rate for ADHD among monozygotic twins compared with dizygotic twins. To date, molecular genetic research has focused on candidate genes in the dopaminergic system. Genes studied include the D2A1 allele of the dopamine D2 receptor gene, the dopamine transporter gene, and the dopamine D4 receptor gene. One of the major limitations to the study of the genetics of behavioral disorders in children has been the overlap among syndromes, including oppositional defiant disorder, conduct disorder, persistent (adult) ADHD, and bipolar disorder. Future research must address weaknesses in existing studies, including small samples sizes, restricted statistical power, and confounding factors such as comorbid illnesses, clinical heterogeneity with variable symptom severity, and unclear phenotypic boundaries.


2021 ◽  
pp. 1-13
Author(s):  
Isabell Brikell ◽  
Christie Burton ◽  
Nina Roth Mota ◽  
Joanna Martin

Abstract Attention-deficit/hyperactivity disorder (ADHD) is a common and highly heritable neurodevelopmental disorder (NDD). In this narrative review, we summarize recent advances in quantitative and molecular genetic research from the past 5–10 years. Combined with large-scale international collaboration, these advances have resulted in fast-paced progress in understanding the etiology of ADHD and how genetic risk factors map on to clinical heterogeneity. Studies are converging on a number of key insights. First, ADHD is a highly polygenic NDD with a complex genetic architecture encompassing risk variants across the spectrum of allelic frequencies, which are implicated in neurobiological processes. Second, genetic studies strongly suggest that ADHD diagnosis shares a large proportion of genetic risks with continuously distributed traits of ADHD in the population, with shared genetic risks also seen across development and sex. Third, ADHD genetic risks are shared with those implicated in many other neurodevelopmental, psychiatric and somatic phenotypes. As sample sizes and the diversity of genetic studies continue to increase through international collaborative efforts, we anticipate further success with gene discovery, characterization of how the ADHD phenotype relates to other human traits and growing potential to use genomic risk factors for understanding clinical trajectories and for precision medicine approaches.


2006 ◽  
Vol 40 (8) ◽  
pp. 639-647 ◽  
Author(s):  
Nick Haslam ◽  
Ben Williams ◽  
Margot Prior ◽  
Ric Haslam ◽  
Brian Graetz ◽  
...  

Objective: To test whether the latent structure of attention deficit/hyperactivity disorder (ADHD) is best understood as categorical or dimensional in samples of 1774 children (aged 6–12 years) and 1222 adolescents (aged 13–17 years) drawn from an Australian epidemiological study. Method: Two taxometric procedures (MAXEIG and MAMBAC) examined ADHD symptom measures assessed by diagnostic interview and parental ratings. Results: Consistent with behavioural genetic research, findings fail to support the view that a latent category underpins ADHD. Conclusions: ADHD is best modelled as a continuum among both children and adolescents, and no discrete dysfunction can therefore be assumed to cause it. The placement of the diagnostic threshold should therefore be decided on pragmatic grounds (e.g. impairment or need for treatment).


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