DNA pooling analysis of ADHD and genes regulating vesicle release of neurotransmitters

Knight, Jo; Xu, Xunfeng; Asherson, Philip

doi:10.1002/ajmg.b.30216

Cited by 27 publications

(9 citation statements)

References 23 publications

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“…Reuter et al [88] found that higher symptom scores were associated with the MET/MET genotype in German adults who were healthy or diagnosed with eating or substance use disorders and Gothelf [89] documented a 5-fold increased risk for the MET allele in 55 subjects with velocardiofacial syndrome and comorbid ADHD relative to those without comorbid ADHD. The lack of significant results from the IMAGE project [90] is consistent with the negative meta-analysis conducted by Cheuk et al [22]. Although these association studies rule out a simple role for the Val108Met polymorphism in the etiology of ADHD, it is of note that COMT hass been found to be highly upregulated in a rat model of ADHD caused by prenatal exposure to polychlorinated biphenyls [91].…”

Section: Association Studies Of Catecholaminergic Genessupporting

confidence: 64%

Molecular Genetics of Attention Deficit Hyperactivity Disorder

Faraone

Mick

2010

Psychiatric Clinics of North America

563

478

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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.

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Section: Association Studies Of Catecholaminergic Genessupporting

confidence: 64%

Molecular Genetics of Attention Deficit Hyperactivity Disorder

Faraone

Mick

2010

Psychiatric Clinics of North America

563

478

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“…Recently, several additional variants of the noradrenaline transporter have been associated to ADHD [20, 22, 65, 83, 84, 86, 95, 191, 192] and require further attention and more elaborate analyses. One example of such an analysis was already described above, suggesting that variations in the noradrenaline transporter may show effects in the presence of specific variants in the COMT gene (and vice versa), only [140].…”

Section: Noradrenergic Systemmentioning

confidence: 99%

Molecular genetics of attention-deficit/hyperactivity disorder: an overview

Banaschewski

Becker

Scherag

et al. 2010

Eur Child Adolesc Psychiatry

221

157

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As heritability is high in attention-deficit/hyperactivity disorder (ADHD), genetic factors must play a significant role in the development and course of this disorder. In recent years a large number of studies on different candidate genes for ADHD have been published, most have focused on genes involved in the dopaminergic neurotransmission system, such as DRD4, DRD5, DAT1/SLC6A3, DBH, DDC. Genes associated with the noradrenergic (such as NET1/SLC6A2, ADRA2A, ADRA2C) and serotonergic systems (such as 5-HTT/SLC6A4, HTR1B, HTR2A, TPH2) have also received considerable interest. Additional candidate genes related to neurotransmission and neuronal plasticity that have been studied less intensively include SNAP25, CHRNA4, NMDA, BDNF, NGF, NTF3, NTF4/5, GDNF. This review article provides an overview of these candidate gene studies, and summarizes findings from recently published genome-wide association studies (GWAS). GWAS is a relatively new tool that enables the identification of new ADHD genes in a hypothesis-free manner. Although these latter studies could be improved and need to be replicated they are starting to implicate processes like neuronal migration and cell adhesion and cell division as potentially important in the aetiology of ADHD and have suggested several new directions for future ADHD genetics studies.

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“…Researchers have mainly studied a functional 48bp variable number of tandem repeats (VNTR) in exon 3 of the DRD4 gene, and have found consistent associations between ADHD and the 7 repeat allele (7R), which is related to decreased functional activity [Asghari et al, ], in both children and adults [Johansson et al, ; Gizer et al, ; Nikolaidis and Gray, ; Sánchez‐Mora et al, ; Tovo‐Rodrigues et al, , 2013]. A second polymorphism in DRD4 , a 120bp duplication located 1.2 kb upstream from the translation start codon that may play a role in transcriptional activity [Paredes et al, ], has also been studied in ADHD with controversial results [Barr et al, ; D'Souza et al, ; Brookes et al, ; Bidwell et al, , Hasler et al, ]…”

Section: Introductionmentioning

confidence: 99%

Dopamine receptor DRD4 gene and stressful life events in persistent attention deficit hyperactivity disorder

Sánchez-Mora

Richarte

Garcia-Martínez

et al. 2015

American J of Med Genetics Pt B

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We performed a case-control association study in persistent ADHD considering eight candidate genes (DRD4, DAT1/ SLC6A3, COMT, ADRA2A, CES1, CYP2D6, LPHN3, and OPRM1) and found additional evidence for the involvement of the Dup 120bp and VNTR 48bp functional variants within the dopamine receptor DRD4 gene in the etiology of adult ADHD. We subsequently investigated the interaction of stressful life events with these two DRD4 polymorphisms, and the impact of such events on the severity of ADHD symptomatology. The gene-by-environment analysis revealed an independent effect of stressful experiences on the severity of persistent ADHD, and a gene-by-environment interaction on the inattentive dimension 480Neuropsychiatric Genetics of the disorder, where non carriers of the Dup 120bp (L) -VNTR 48bp (7R) haplotype were more sensitive to environmental adversity than carriers. These results are in agreement with previous works reporting a relationship between DRD4 and the effect of adverse experiences, which may explain the discordant findings in previous genetic studies and strengthen the importance of gene-by-environment interactions on the severity of ADHD. Ó 2015 Wiley Periodicals, Inc.

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DNA pooling analysis of ADHD and genes regulating vesicle release of neurotransmitters

Cited by 27 publications

References 23 publications

Molecular Genetics of Attention Deficit Hyperactivity Disorder

Molecular Genetics of Attention Deficit Hyperactivity Disorder

Molecular genetics of attention-deficit/hyperactivity disorder: an overview

Dopamine receptor DRD4 gene and stressful life events in persistent attention deficit hyperactivity disorder

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