Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD)
Evangelia Stergiakouli, Anita ThaparDepartment of Psychological Medicine and Neurology, MRC Centre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, United KingdomAbstract: Attention-deficit/hyperactivity disorder (ADHD) is a highly disruptive childhood-onset disord...
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Dove Medical Press
2010
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oai:doaj.org-article:b9ae41ef650d4e3cb801e440269cffa12021-12-02T07:09:34ZFitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD)1176-63281178-2021https://doaj.org/article/b9ae41ef650d4e3cb801e440269cffa12010-08-01T00:00:00Zhttp://www.dovepress.com/fitting-the-pieces-together-current-research-on-the-genetic-basis-of-a-a5101https://doaj.org/toc/1176-6328https://doaj.org/toc/1178-2021Evangelia Stergiakouli, Anita ThaparDepartment of Psychological Medicine and Neurology, MRC Centre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, United KingdomAbstract: Attention-deficit/hyperactivity disorder (ADHD) is a highly disruptive childhood-onset disorder that often persists into adolescence and adulthood. Comorbidity with other problems, such as autism, dyslexia and conduct disorder (CD) is very common. Although little is known about the pathophysiology of ADHD, family, twin and adoption studies have shown that it is highly heritable. Whole genome linkage studies suggest there are no common susceptibility genes of moderate effect size. Most published research has been based on functional candidate gene studies. The most consistent evidence for association with ADHD relates to a dopamine D4 receptor (DRD4) gene variable number tandem repeat (VNTR), a dopamine D5 receptor (DRD5) gene microsatellite and a dopamine transporter (DAT1) gene VNTR. In addition, the catechol-O-methyltransferase (COMT) val158/108 met variant has been shown to increase risk for associated antisocial behavior. The first genome-wide association studies (GWAS) of ADHD have been completed and although larger studies are still required to detect common risk variants, novel risk pathways are being suggested for ADHD. Further research on the contribution of rare variants, larger genome-wide association and sequencing studies and ADHD phenotype refinement is now needed.Keywords: attention-deficit/hyperactivity disorder (ADHD), genetics, molecular genetics, genome-wide association study (GWAS), gene-environment interplay Evangelia StergiakouliAnita ThaparDove Medical PressarticleNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol 2010, Iss Issue 1, Pp 551-560 (2010) |
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Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 |
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Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Evangelia Stergiakouli Anita Thapar Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD) |
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Evangelia Stergiakouli, Anita ThaparDepartment of Psychological Medicine and Neurology, MRC Centre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, United KingdomAbstract: Attention-deficit/hyperactivity disorder (ADHD) is a highly disruptive childhood-onset disorder that often persists into adolescence and adulthood. Comorbidity with other problems, such as autism, dyslexia and conduct disorder (CD) is very common. Although little is known about the pathophysiology of ADHD, family, twin and adoption studies have shown that it is highly heritable. Whole genome linkage studies suggest there are no common susceptibility genes of moderate effect size. Most published research has been based on functional candidate gene studies. The most consistent evidence for association with ADHD relates to a dopamine D4 receptor (DRD4) gene variable number tandem repeat (VNTR), a dopamine D5 receptor (DRD5) gene microsatellite and a dopamine transporter (DAT1) gene VNTR. In addition, the catechol-O-methyltransferase (COMT) val158/108 met variant has been shown to increase risk for associated antisocial behavior. The first genome-wide association studies (GWAS) of ADHD have been completed and although larger studies are still required to detect common risk variants, novel risk pathways are being suggested for ADHD. Further research on the contribution of rare variants, larger genome-wide association and sequencing studies and ADHD phenotype refinement is now needed.Keywords: attention-deficit/hyperactivity disorder (ADHD), genetics, molecular genetics, genome-wide association study (GWAS), gene-environment interplay |
format |
article |
author |
Evangelia Stergiakouli Anita Thapar |
author_facet |
Evangelia Stergiakouli Anita Thapar |
author_sort |
Evangelia Stergiakouli |
title |
Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD) |
title_short |
Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD) |
title_full |
Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD) |
title_fullStr |
Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD) |
title_full_unstemmed |
Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD) |
title_sort |
fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (adhd) |
publisher |
Dove Medical Press |
publishDate |
2010 |
url |
https://doaj.org/article/b9ae41ef650d4e3cb801e440269cffa1 |
work_keys_str_mv |
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