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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies</title>
<author><name sortKey="Kebir, Oussama" sort="Kebir, Oussama" uniqKey="Kebir O" first="Oussama" last="Kebir">Oussama Kebir</name>
</author>
<author><name sortKey="Tabbane, Karim" sort="Tabbane, Karim" uniqKey="Tabbane K" first="Karim" last="Tabbane">Karim Tabbane</name>
</author>
<author><name sortKey="Sengupta, Sarojini" sort="Sengupta, Sarojini" uniqKey="Sengupta S" first="Sarojini" last="Sengupta">Sarojini Sengupta</name>
</author>
<author><name sortKey="Joober, Ridha" sort="Joober, Ridha" uniqKey="Joober R" first="Ridha" last="Joober">Ridha Joober</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">19270759</idno>
<idno type="pmc">2647566</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647566</idno>
<idno type="RBID">PMC:2647566</idno>
<date when="2009">2009</date>
<idno type="wicri:Area/Pmc/Corpus">000104</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000104</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies</title>
<author><name sortKey="Kebir, Oussama" sort="Kebir, Oussama" uniqKey="Kebir O" first="Oussama" last="Kebir">Oussama Kebir</name>
</author>
<author><name sortKey="Tabbane, Karim" sort="Tabbane, Karim" uniqKey="Tabbane K" first="Karim" last="Tabbane">Karim Tabbane</name>
</author>
<author><name sortKey="Sengupta, Sarojini" sort="Sengupta, Sarojini" uniqKey="Sengupta S" first="Sarojini" last="Sengupta">Sarojini Sengupta</name>
</author>
<author><name sortKey="Joober, Ridha" sort="Joober, Ridha" uniqKey="Joober R" first="Ridha" last="Joober">Ridha Joober</name>
</author>
</analytic>
<series><title level="j">Journal of Psychiatry & Neuroscience : JPN</title>
<idno type="ISSN">1180-4882</idno>
<idno type="eISSN">1488-2434</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>We reviewed systematically the results of genetic studies investigating associations between putative susceptibility genes for attention-deficit hyperactivity disorder (ADHD) and neuropsychological traits relevant for this disorder.</p>
</sec>
<sec><title>Methods</title>
<p>We identified papers for review through the PubMed database.</p>
</sec>
<sec><title>Results</title>
<p>Twenty-nine studies examined 10 genes (DRD4, DAT1, COMT, DBH, MAOA, DRD5, ADRA2A, GRIN2A, BDNF and TPH2) in relation to neuropsychological traits relevant for ADHD. For DRD4, the continuous performance test (CPT) and derived tasks were the most used tests. Association of high reaction time variability with the 7-repeat allele absence appears to be the most consistent result and seems to be specific to ADHD. Speed of processing, set-shifting and cognitive impulsiveness were less frequently investigated but seem to be altered in the 7-repeat allele carriers. No effect of genotype was found on response inhibition (the stop and go/no-go tasks). For DAT1, 4 studies provide conflicting results in relation to omission and commission errors from CPT and derived tasks. High reaction time variability seems to be the most replicated cognitive marker associated with the 10-repeat homozygosity. The other genes have attracted fewer studies, and the reported findings need to be replicated.</p>
</sec>
<sec><title>Limitations</title>
<p>Although we aimed to perform a formal meta-analysis, this was not possible because the number of studies using the same neurocognitive endophenotypes was limited. We referred only minimally to the various theoretical frameworks in this field of research; more detail would have been beyond the scope of our systematic review. Finally, sample sizes in most of the studies we reviewed were small. Thus, some negative findings could be attributed to a lack of statistical power, and positive results should be considered preliminary until they are replicated in extended samples.</p>
</sec>
<sec><title>Conclusion</title>
<p>Several methodological issues, including measurement errors, developmental changes in cognitive abilities, sex, psychostimulant effects and presence of comorbid conditions, represent confounding factors and may explain conflicting results.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Psychiatry Neurosci</journal-id>
<journal-title>Journal of Psychiatry & Neuroscience : JPN</journal-title>
<issn pub-type="ppub">1180-4882</issn>
<issn pub-type="epub">1488-2434</issn>
<publisher><publisher-name>Canadian Medical Association</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">19270759</article-id>
<article-id pub-id-type="pmc">2647566</article-id>
<article-id pub-id-type="publisher-id">0001585-200903000-00002</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review Paper</subject>
</subj-group>
</article-categories>
<title-group><article-title>Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Kebir</surname>
<given-names>Oussama</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Tabbane</surname>
<given-names>Karim</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Sengupta</surname>
<given-names>Sarojini</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Joober</surname>
<given-names>Ridha</given-names>
</name>
</contrib>
</contrib-group>
<aff>Kebir, Tabbane — Research unit “Cognitive dysfunctions in psychiatric diseases,” Razi Hospital, La Manouba, Tunisia; Sengupta, Joober — Department of Psychiatry, McGill University, and Douglas Hospital Research Centre, Montréal, Que.<break></break>
</aff>
<pub-date pub-type="ppub"><month>3</month>
<year>2009</year>
</pub-date>
<volume>34</volume>
<issue>2</issue>
<fpage>88</fpage>
<lpage>101</lpage>
<copyright-statement>© 2009 Canadian Medical Association or its licensors</copyright-statement>
<abstract><sec><title>Background</title>
<p>We reviewed systematically the results of genetic studies investigating associations between putative susceptibility genes for attention-deficit hyperactivity disorder (ADHD) and neuropsychological traits relevant for this disorder.</p>
</sec>
<sec><title>Methods</title>
<p>We identified papers for review through the PubMed database.</p>
</sec>
<sec><title>Results</title>
<p>Twenty-nine studies examined 10 genes (DRD4, DAT1, COMT, DBH, MAOA, DRD5, ADRA2A, GRIN2A, BDNF and TPH2) in relation to neuropsychological traits relevant for ADHD. For DRD4, the continuous performance test (CPT) and derived tasks were the most used tests. Association of high reaction time variability with the 7-repeat allele absence appears to be the most consistent result and seems to be specific to ADHD. Speed of processing, set-shifting and cognitive impulsiveness were less frequently investigated but seem to be altered in the 7-repeat allele carriers. No effect of genotype was found on response inhibition (the stop and go/no-go tasks). For DAT1, 4 studies provide conflicting results in relation to omission and commission errors from CPT and derived tasks. High reaction time variability seems to be the most replicated cognitive marker associated with the 10-repeat homozygosity. The other genes have attracted fewer studies, and the reported findings need to be replicated.</p>
</sec>
<sec><title>Limitations</title>
<p>Although we aimed to perform a formal meta-analysis, this was not possible because the number of studies using the same neurocognitive endophenotypes was limited. We referred only minimally to the various theoretical frameworks in this field of research; more detail would have been beyond the scope of our systematic review. Finally, sample sizes in most of the studies we reviewed were small. Thus, some negative findings could be attributed to a lack of statistical power, and positive results should be considered preliminary until they are replicated in extended samples.</p>
</sec>
<sec><title>Conclusion</title>
<p>Several methodological issues, including measurement errors, developmental changes in cognitive abilities, sex, psychostimulant effects and presence of comorbid conditions, represent confounding factors and may explain conflicting results.</p>
</sec>
</abstract>
<trans-abstract xml:lang="FR"><sec><title>Contexte</title>
<p>Nous avons revu systématiquement des résultats des études génétiques ayant examiné l'association entre des gènes de susceptibilité au trouble hyperactivité/déficit de l'attention (THADA) et les marqueurs neuropsychologiques les plus incriminés dans ce trouble.</p>
</sec>
<sec><title>Méthodes</title>
<p>Nous avons recueilli des articles analysés dans cette revue par le moyen d'interrogation de la base de données PubMed.</p>
</sec>
<sec><title>Résultats</title>
<p>Vingt-neuf études ont examiné 10 gènes (DRD4, DAT1, COMT, DBH, MAOA, DRD5, ADRA2A, GRIN2A, BDNF et TPH2) en association aux traits neuropsychologiques impliqués dans le THADA. Pour DRD4, le « continuous performance test » (CPT) et les tâches dérivées représentent les tâches les plus utilizées. L'association d'une grande variabilité des temps de réaction avec l'absence de l'allèle « 7-repeat » apparaît comme le résultat le plus solide et semble être spécifique au THADA. La vitesse de traitement, la flexibilité et l'impulsivité cognitives ont été moins fréquemment étudiées mais semblent être perturbées chez les porteurs de l'allèle « 7-repeat ». Il n'existe pas d'effet du génotype sur la capacité d'inhibition (tâches stop et go/no-go). Pour DAT1, 4 études rapportent des résultats discordants concernant les erreurs d'omission et de commission au CPT et tâches dérivées. Une grande variabilité des temps de réaction semble être le marqueur cognitif le plus répliqué en association à l'homozygosité de l'allèle « 10-repeat ». Les autres gènes ont fait l'objet de moins d'études dont les résultats nécessitent des réplications.</p>
</sec>
<sec><title>Limites</title>
<p>Une méta-analyse n'a pas pu être réalisée vu le faible nobre d'études utilisant le même endophénotype cognitif. Nous nous sommes référés au minimum aux différentes approches théoriques dans ce champ de recherche car les aborder en détail aurait dépassé l'objectif de cette étude d'examen critique. Enfin, les échantillons étudiés sont de petite taille. De ce fait, quelques résultats négatifs pourraient être attribués au manque de puissance statistique et les associations positives devraient être considérées comme préliminaires jusqu'à leur réplication dans des échantillons plus grands.</p>
</sec>
<sec><title>Conclusion</title>
<p>Plusieurs problèmes méthodologiques incluant les erreurs de mesure, l'effet du développement sur les performances cognitives, le sexe, les effets des traitements psychostimulants et la présence de comorbidités sont relevés. Ils représentent des facteurs confondants et peuvent contribuer à la discordance des résultats.</p>
</sec>
</trans-abstract>
</article-meta>
</front>
</pmc>
</record>
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