Lack of association of the dopamine transporter gene in a French ADHD sample

Wohl, M.; Boni, Claudette; Asch, M. van; Cortese, Samuele; Orejarena, Silvia; Mouren, Marie Christine; Gorwood, Philip; Purper-Ouakil, Diane

doi:10.1002/ajmg.b.30695

Cited by 20 publications

(16 citation statements)

References 11 publications

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“…First, our sample size was much larger than any of the published studies examining cognitive function in ADHD and DBH (sample sizes ranging from 54 to 122) [Barkley et al, 2006; Bellgrove et al, 2006b; Kieling et al, 2008], which provided greater power to examine possible genotypic effects. Second, we performed all the analyses after controlling possible confounding from IQ, which was not done in some of the previous studies [Bellgrove et al, 2005, 2006b; Kieling et al, 2006; Wohl et al, 2008]. With regard to limitations, the first one is that the cases and unaffected controls were not perfectly matched, with IQ slightly, but significantly, higher in the healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Miscibility, crystallization kinetics, and mechanical properties of poly(3‐hydroxybutyrate‐co‐3‐hydroxyvalerate)(PHBV)/poly(3‐hydroxybutyrate‐co‐4‐hydroxybutyrate)(P3/4HB) blends

Wang

Chen

et al. 2010

J of Applied Polymer Sci

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Poly(3-hydroxybutyrate-co-3-hydroxyvalerate)(PHBV)/poly(3-hydroxybutyrate-co-4-hydroxybutyrate) (P3/4HB) blend films were prepared by solvent-cast method. The nonisothermal crystallization results showed that PHBV and P3/4HB are miscible due to a single glass transition temperature (T g ), which is dependent on blend composition. The isothermal crystallization results demonstrate that the crystallization rate of PHBV becomes slower after adding amorphous P3/4HB with 19.2 mol% 4HB, which could be proved through depression of equilibrium melt point (T C and 84 C, respectively. FTIR analysis showed that PHBV/P3/4HB blend films would maintain the helical structure, similar to pure PHBV. Meanwhile, with increasing P3/4HB content, the inter-and intrainteractions of PHBV and P3/4HB decrease gradually. Besides, a lower elastic modulus and a higher elongation at break were obtained, which show that the addition of P3/ 4HB would make the brittle PHBV to ductile materials.

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Section: Discussionmentioning

confidence: 99%

Miscibility, crystallization kinetics, and mechanical properties of poly(3‐hydroxybutyrate‐co‐3‐hydroxyvalerate)(PHBV)/poly(3‐hydroxybutyrate‐co‐4‐hydroxybutyrate)(P3/4HB) blends

Wang

Chen

et al. 2010

J of Applied Polymer Sci

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“…Association studies in ADHD offer conflicting data [86–91]. Kebir et al [92] identified 29 studies that examined 10 genes (DRD4, DAT1, COMT, DBH, MAOA, DRD5, ADRA2A, GRIN2A, BDNF, TPH2) in relation to neuropsychological traits (endophenotypes) that were relevant for ADHD, in this case with difficulties involving Continuous Performance Test variables.…”

Section: Epigenetics In Adhdmentioning

confidence: 99%

Epigenetics in Developmental Disorder: ADHD and Endophenotypes

Archer

Oscar‐Berman²,

Blum³

2011

J Genet Syndr Gene Ther

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Heterogeneity in attention-deficit/hyperactivity disorder (ADHD), with complex interactive operations of genetic and environmental factors, is expressed in a variety of disorder manifestations: severity, co-morbidities of symptoms, and the effects of genes on phenotypes. Neurodevelopmental influences of genomic imprinting have set the stage for the structuralphysiological variations that modulate the cognitive, affective, and pathophysiological domains of ADHD. The relative contributions of genetic and environmental factors provide rapidly proliferating insights into the developmental trajectory of the condition, both structurally and functionally. Parent-of-origin effects seem to support the notion that genetic risks for disease process debut often interact with the social environment, i.e., the parental environment in infants and young children. The notion of endophenotypes, markers of an underlying liability to the disorder, may facilitate detection of genetic risks relative to a complex clinical disorder. Simple genetic association has proven insufficient to explain the spectrum of ADHD. At a primary level of analysis, the consideration of epigenetic regulation of brain signalling mechanisms, dopamine, serotonin, and noradrenaline is examined. Neurotrophic factors that participate in the neurogenesis, survival, and functional maintenance of brain systems, are involved in neuroplasticity alterations underlying brain disorders, and are implicated in the genetic predisposition to ADHD, but not obviously, nor in a simple or straightforward fashion. In the context of intervention, genetic linkage studies of ADHD pharmacological intervention have demonstrated that associations have fitted the "drug response phenotype," rather than the disorder diagnosis. Despite conflicting evidence for the existence, or not, of genetic associations between disorder diagnosis and genes regulating the structure and function of neurotransmitters and brainderived neurotrophic factor (BDNF), associations between symptoms-profiles endophenotypes and single nucleotide polymorphisms appear reassuring.

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“…However, Li et al did find significant evidence of heterogeneity, with greater evidence for positive association from family-based studies and European studies compared to case-control studies and Asian studies. Not included in these meta-analyses are recent studies, some supporting the DAT1 association with ADHD [Henr ıquez et al, 2008;Kopeckov a et al, 2008], and some not [Wang et al, 2008;Wohl et al, 2008].…”

Section: Introductionmentioning

confidence: 97%

ADHD and DAT1: Further evidence of paternal over‐transmission of risk alleles and haplotype

Hawi

Kent

Hill

et al. 2009

American J of Med Genetics Pt B

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We [Hawi et al. (2005); Am J Hum Genet 77:958-965] reported paternal over-transmission of risk alleles in some ADHD-associated genes. This was particularly clear in the case of the DAT1 3'-UTR VNTR. In the current investigation, we analyzed three new sample comprising of 1,248 ADHD nuclear families to examine the allelic over-transmission of DAT1 in ADHD. The IMAGE sample, the largest of the three-replication samples, provides strong support for a parent of origin effect for allele 6 and the 10 repeat allele (intron 8 and 3'-UTR VNTR, respectively) of DAT1. In addition, a similar pattern of over-transmission of paternal risk haplotypes (constructed from the above alleles) was also observed. Some support is also derived from the two smaller samples although neither is independently significant. Although the mechanism driving the paternal over-transmission of the DAT risk alleles is not known, these finding provide further support for this phenomenon.

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Lack of association of the dopamine transporter gene in a French ADHD sample

Cited by 20 publications

References 11 publications

Miscibility, crystallization kinetics, and mechanical properties of poly(3‐hydroxybutyrate‐co‐3‐hydroxyvalerate)(PHBV)/poly(3‐hydroxybutyrate‐co‐4‐hydroxybutyrate)(P3/4HB) blends

Miscibility, crystallization kinetics, and mechanical properties of poly(3‐hydroxybutyrate‐co‐3‐hydroxyvalerate)(PHBV)/poly(3‐hydroxybutyrate‐co‐4‐hydroxybutyrate)(P3/4HB) blends

Epigenetics in Developmental Disorder: ADHD and Endophenotypes

ADHD and DAT1: Further evidence of paternal over‐transmission of risk alleles and haplotype

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