Sirvi Märksõna "ADHD" järgi

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ADHD co-morbidities: A review of implication of gene × environment effects with dopamine-related genes
(2022) Kanarik, Margus; Grimm, Oliver; Mota, Nina Roth; Reif, Andreas; Harro, Jaanus
ADHD is a major burden in adulthood, where co-morbid conditions such as depression, substance use disorder and obesity often dominate the clinical picture. ADHD has substantial shared heritability with other mental disorders, contributing to comorbidity. However, environmental risk factors exist but their interaction with genetic makeup, especially in relation to comorbid disorders, remains elusive. This review for the first time summarizes present knowledge on gene x environment (GxE) interactions regarding the dopamine system. Hitherto, mainly candidate (GxE) studies were performed, focusing on the genes DRD4, DAT1 and MAOA. Some evidence suggest that the DRD4 exon 3 variable number tandem repeat (VNTR) and MAOA uVNTR may mediate (GxE) interactions in ADHD generally, and comorbid conditions specifically. For other polymorphisms, evidence is contradictory and less convincing. Particularly lacking are longitudinal studies testing the interaction of well-defined environmental with polygenic risk scores reflecting the dopamine system in its entirety. Only such an approach would be less susceptible to false-positive findings and provide clues on how genes could interact with non-genetic factors to shape psychopathology over the life span.
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Driving risks of young drivers with symptoms of attention deficit hyperactivity disorder: association with the dopamine transporter gene VNTR polymorphism
(2022) Tokko, Tõnis; Eensoo, Diva; Miškinyte, Grete; Harro, Jaanus
Road traffic injuries are a leading cause of death for young adults, and young drivers with higher expression of symptoms of attention deficit-hyperactivity disorder (ADHD) could pose an even greater risk in traffic. Dopaminergic dysfunction has been found to occur in ADHD, with the dopamine transporter (DAT) gene VNTR polymorphism (DAT1 VNTR; rs28363170) being one of the most consistent genetic markers. Thus, we aimed at clarifying how the ADHD symptoms and the DAT1 VNTR relate to risk-taking behaviour in traffic, impulsivity and driving anger in young drivers. We used data of two traffic behaviour study samples (n = 741, mean age = 23.3±7.2 years; n = 995, mean age = 22.9±8.1 years) and the Estonian Children Personality Behaviour and Health Study (ECPBHS; traffic behaviour data n = 1016, mean age = 25.2±2.1 years). ADHD symptoms were assessed by self-report with the Adult ADHD Self-Report Scale (ASRS v1.1) and impulsivity with the Adaptive and Maladaptive Impulsivity Scale. Traffic behavioural measures were either self-reported (Driver Behaviour Questionnaire, Driving Anger Scale) or obtained from databases (registered accidents and violations). Drivers with more self-reported ADHD symptoms also reported more risk-taking in traffic and had more of recorded traffic accidents and violations. DAT1 9R carriers had a higher probability of high traffic risk behaviour only if they also had ADHD symptoms. Conclusion Higher level of ADHD symptoms is a significant risk factor in traffic, and carrying of the DAT1 9R allele appears to aggravate these risks.
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Driving risks of young drivers with symptoms of attention deficit hyperactivity disorder: association with the dopamine transporter gene VNTR polymorphism
(2022) Tokko, Tõnis; Eensoo, Diva; Miškinyte, Grete; Harro, Jaanus
Background: Road traffic injuries are a leading cause of death for young adults, and young drivers with higher expression of symptoms of attention deficit-hyperactivity disorder (ADHD) could pose an even greater risk in traffic. Dopaminergic dysfunction has been found to occur in ADHD, with the dopamine transporter (DAT) gene VNTR polymorphism (DAT1 VNTR; rs28363170) being one of the most consistent genetic markers. Thus, we aimed at clarifying how the ADHD symptoms and the DAT1 VNTR relate to risk-taking behaviour in traffic, impulsivity and driving anger in young drivers. Method: We used data of two traffic behaviour study samples (n = 741, mean age = 23.3±7.2 years; n = 995, mean age = 22.9±8.1 years) and the Estonian Children Personality Behaviour and Health Study (ECPBHS; traffic behaviour data n = 1016, mean age = 25.2±2.1 years). ADHD symptoms were assessed by self-report with the Adult ADHD Self-Report Scale (ASRS v1.1) and impulsivity with the Adaptive and Maladaptive Impulsivity Scale. Traffic behavioural measures were either self-reported (Driver Behaviour Questionnaire, Driving Anger Scale) or obtained from databases (registered accidents and violations). Results: Drivers with more self-reported ADHD symptoms also reported more risk-taking in traffic and had more of recorded traffic accidents and violations. DAT1 9R carriers had a higher probability of high traffic risk behaviour only if they also had ADHD symptoms. Conclusion: Higher level of ADHD symptoms is a significant risk factor in traffic, and carrying of the DAT1 9R allele appears to aggravate these risks.
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Kontrollitud tähelepanu hoidmise treeningu ülekandeefekt tähelepanu suunamise efektiivsusele
(Tartu Ülikool, 2025) Jadrina, Marija; Tuvi, Iiris, juhendaja; Tartu Ülikool. Sotsiaalteaduste valdkond; Tartu Ülikool. Psühholoogia instituut
Käesoleva pilootuuringu eesmärgiks oli uurida endogeense tähelepanu hoidmise treenimise tõhusust ja selle mõju nii endogeense kui eksogeense tähelepanu suunamisele. Töö peamiseks hüpoteesiks oli see, et tähelepanu hoidmise treening suurendab endogeense tähelepanu suunamise efektiivsust samas kui eksogeense tähelepanu suunamise efektiivsus ei muutu. Hüpoteesi testimiseks kasutati segatüüpi katseplaani, kuna kombineeriti nii sõltuvate kui sõltumatute muutujate katseplaani baastaseme mõõtmisega. Esiteks, mõõdeti 13 katseisiku endogeense ja eksogeense tähelepanu ulatust kasutades tähelepanu suunamise katset. Teiseks, 6 inimesest koosnev eksperimentaalgrupp sai kolm tähelepanu hoidmise treeningut ühe nädala jooksul. Lõpuks, mõõdeti tähelepanu ulatuse taaskord ning analüüsiti tähelepanu hoidmise treeningute efektiivsust. Uuringu tulemustest selgus, et endogeense tähelepanu treening ei omanud statistiliselt olulist efekti endogeense tähelepanu ulatuse suurendamisele ega eksogeense tähelepanu ulatuse muutmisele.