Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets / Merel C. POSTEMA in Journal of Child Psychology and Psychiatry, 62-10 (October 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1202-1219 Titre : Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets Type de document : Texte imprimé et/ou numérique Auteurs : Merel C. POSTEMA, Auteur ; Martine HOOGMAN, Auteur ; Sara AMBROSINO, Auteur ; Philip ASHERSON, Auteur ; Tobias BANASCHEWSKI, Auteur ; Cibele E. BANDEIRA, Auteur ; Alexandr BARANOV, Auteur ; Claiton H.D. BAU, Auteur ; Sarah BAUMEISTER, Auteur ; Ramona BAUR-STREUBEL, Auteur ; Mark A. BELLGROVE, Auteur ; Joseph BIEDERMAN, Auteur ; Janita B. BRALTEN, Auteur ; Daniel BRANDEIS, Auteur ; Silvia BREM, Auteur ; Jan K. BUITELAAR, Auteur ; Geraldo F. BUSATTO, Auteur ; Francisco Xavier CASTELLANOS, Auteur ; Mara CERCIGNANI, Auteur ; Tiffany M. CHAIM-AVANCINI, Auteur ; Kaylita C. CHANTILUKE, Auteur ; Anastasia CHRISTAKOU, Auteur ; David COGHILL, Auteur ; Annette CONZELMANN, Auteur ; Ana I. CUBILLO, Auteur ; Renata B. CUPERTINO, Auteur ; Patrick DE ZEEUW, Auteur ; Alysa E. DOYLE, Auteur ; Sarah DURSTON, Auteur ; Eric A. EARL, Auteur ; Jeffery N. EPSTEIN, Auteur ; Thomas ETHOFER, Auteur ; Damien A. FAIR, Auteur ; Andreas J. FALLGATTER, Auteur ; Stephen V. FARAONE, Auteur ; Thomas FRODL, Auteur ; Matt C. GABEL, Auteur ; Tinatin GOGBERASHVILI, Auteur ; Eugenio H. GREVET, Auteur ; Jan HAAVIK, Auteur ; Neil A. HARRISON, Auteur ; Catharina A. HARTMAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Sarah HOHMANN, Auteur ; Marie F. HØVIK, Auteur ; Terry L. JERNIGAN, Auteur ; Bernd KARDATZKI, Auteur ; Georgii KARKASHADZE, Auteur ; Clare KELLY, Auteur ; Gregor KOHLS, Auteur ; Kerstin KONRAD, Auteur ; Jonna KUNTSI, Auteur ; Luisa LÁZARO, Auteur ; Sara LERA-MIGUEL, Auteur ; Klaus-Peter LESCH, Auteur ; Mario R. LOUZA, Auteur ; Astri J. LUNDERVOLD, Auteur ; Charles B MALPAS, Auteur ; Paulo MATTOS, Auteur ; Hazel MCCARTHY, Auteur ; Leyla NAMAZOVA-BARANOVA, Auteur ; Rosa NICOLAU, Auteur ; Joel T. NIGG, Auteur ; Stephanie E. NOVOTNY, Auteur ; Eileen OBERWELLAND WEISS, Auteur ; Ruth L. O'GORMAN TUURA, Auteur ; Jaap OOSTERLAAN, Auteur ; Bob ORANJE, Auteur ; Yannis PALOYELIS, Auteur ; Paul PAULI, Auteur ; Felipe A. PICON, Auteur ; Kerstin J. PLESSEN, Auteur ; J. Antoni RAMOS-QUIROGA, Auteur ; Andreas REIF, Auteur ; Liesbeth RENEMAN, Auteur ; Pedro G.P. ROSA, Auteur ; Katya RUBIA, Auteur ; Anouk SCHRANTEE, Auteur ; Lizanne SCHWEREN, Auteur ; Jochen SEITZ, Auteur ; Philip SHAW, Auteur ; Tim J. SILK, Auteur ; Norbert SKOKAUSKAS, Auteur ; Juan C. SOLIVA VILA, Auteur ; Michael C. STEVENS, Auteur ; Gustavo SUDRE, Auteur ; Leanne TAMM, Auteur ; Fernanda TOVAR-MOLL, Auteur ; Theo G.M. VAN ERP, Auteur ; Alasdair VANCE, Auteur ; Oscar VILARROYA, Auteur ; Yolanda VIVES-GILABERT, Auteur ; Georg G. VON POLIER, Auteur ; Susanne WALITZA, Auteur ; Yuliya N. YONCHEVA, Auteur ; Marcus V. ZANETTI, Auteur ; Georg C. ZIEGLER, Auteur ; David C. GLAHN, Auteur ; Neda JAHANSHAD, Auteur Année de publication : 2021 Article en page(s) : p.1202-1219 Langues : Anglais (eng) Mots-clés : Attention-deficit  brain asymmetry  brain laterality  hyperactivity disorder  large-scale data  structural MRI Index. décimale : PER Périodiques Résumé : Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from ?0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait. En ligne : https://doi.org/10.1111/jcpp.13396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=462 [article] Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets [Texte imprimé et/ou numérique] / Merel C. POSTEMA, Auteur ; Martine HOOGMAN, Auteur ; Sara AMBROSINO, Auteur ; Philip ASHERSON, Auteur ; Tobias BANASCHEWSKI, Auteur ; Cibele E. BANDEIRA, Auteur ; Alexandr BARANOV, Auteur ; Claiton H.D. BAU, Auteur ; Sarah BAUMEISTER, Auteur ; Ramona BAUR-STREUBEL, Auteur ; Mark A. BELLGROVE, Auteur ; Joseph BIEDERMAN, Auteur ; Janita B. BRALTEN, Auteur ; Daniel BRANDEIS, Auteur ; Silvia BREM, Auteur ; Jan K. BUITELAAR, Auteur ; Geraldo F. BUSATTO, Auteur ; Francisco Xavier CASTELLANOS, Auteur ; Mara CERCIGNANI, Auteur ; Tiffany M. CHAIM-AVANCINI, Auteur ; Kaylita C. CHANTILUKE, Auteur ; Anastasia CHRISTAKOU, Auteur ; David COGHILL, Auteur ; Annette CONZELMANN, Auteur ; Ana I. CUBILLO, Auteur ; Renata B. CUPERTINO, Auteur ; Patrick DE ZEEUW, Auteur ; Alysa E. DOYLE, Auteur ; Sarah DURSTON, Auteur ; Eric A. EARL, Auteur ; Jeffery N. EPSTEIN, Auteur ; Thomas ETHOFER, Auteur ; Damien A. FAIR, Auteur ; Andreas J. FALLGATTER, Auteur ; Stephen V. FARAONE, Auteur ; Thomas FRODL, Auteur ; Matt C. GABEL, Auteur ; Tinatin GOGBERASHVILI, Auteur ; Eugenio H. GREVET, Auteur ; Jan HAAVIK, Auteur ; Neil A. HARRISON, Auteur ; Catharina A. HARTMAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Sarah HOHMANN, Auteur ; Marie F. HØVIK, Auteur ; Terry L. JERNIGAN, Auteur ; Bernd KARDATZKI, Auteur ; Georgii KARKASHADZE, Auteur ; Clare KELLY, Auteur ; Gregor KOHLS, Auteur ; Kerstin KONRAD, Auteur ; Jonna KUNTSI, Auteur ; Luisa LÁZARO, Auteur ; Sara LERA-MIGUEL, Auteur ; Klaus-Peter LESCH, Auteur ; Mario R. LOUZA, Auteur ; Astri J. LUNDERVOLD, Auteur ; Charles B MALPAS, Auteur ; Paulo MATTOS, Auteur ; Hazel MCCARTHY, Auteur ; Leyla NAMAZOVA-BARANOVA, Auteur ; Rosa NICOLAU, Auteur ; Joel T. NIGG, Auteur ; Stephanie E. NOVOTNY, Auteur ; Eileen OBERWELLAND WEISS, Auteur ; Ruth L. O'GORMAN TUURA, Auteur ; Jaap OOSTERLAAN, Auteur ; Bob ORANJE, Auteur ; Yannis PALOYELIS, Auteur ; Paul PAULI, Auteur ; Felipe A. PICON, Auteur ; Kerstin J. PLESSEN, Auteur ; J. Antoni RAMOS-QUIROGA, Auteur ; Andreas REIF, Auteur ; Liesbeth RENEMAN, Auteur ; Pedro G.P. ROSA, Auteur ; Katya RUBIA, Auteur ; Anouk SCHRANTEE, Auteur ; Lizanne SCHWEREN, Auteur ; Jochen SEITZ, Auteur ; Philip SHAW, Auteur ; Tim J. SILK, Auteur ; Norbert SKOKAUSKAS, Auteur ; Juan C. SOLIVA VILA, Auteur ; Michael C. STEVENS, Auteur ; Gustavo SUDRE, Auteur ; Leanne TAMM, Auteur ; Fernanda TOVAR-MOLL, Auteur ; Theo G.M. VAN ERP, Auteur ; Alasdair VANCE, Auteur ; Oscar VILARROYA, Auteur ; Yolanda VIVES-GILABERT, Auteur ; Georg G. VON POLIER, Auteur ; Susanne WALITZA, Auteur ; Yuliya N. YONCHEVA, Auteur ; Marcus V. ZANETTI, Auteur ; Georg C. ZIEGLER, Auteur ; David C. GLAHN, Auteur ; Neda JAHANSHAD, Auteur . - 2021 . - p.1202-1219. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1202-1219 Mots-clés : Attention-deficit  brain asymmetry  brain laterality  hyperactivity disorder  large-scale data  structural MRI Index. décimale : PER Périodiques Résumé : Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from ?0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait. En ligne : https://doi.org/10.1111/jcpp.13396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=462

Female-specific association of NOS1 genotype with white matter microstructure in ADHD patients and controls / Hanneke VAN EWIJK in Journal of Child Psychology and Psychiatry, 58-8 (August 2017)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 58-8 (August 2017) . - p.958-966 Titre : Female-specific association of NOS1 genotype with white matter microstructure in ADHD patients and controls Type de document : Texte imprimé et/ou numérique Auteurs : Hanneke VAN EWIJK, Auteur ; Janita B. BRALTEN, Auteur ; Esther D. A. VAN DUIN, Auteur ; Marina HAKOBJAN, Auteur ; Jan K. BUITELAAR, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Catharina A. HARTMAN, Auteur ; Martine HOOGMAN, Auteur ; Jaap OOSTERLAAN, Auteur ; Barbara FRANKE, Auteur Article en page(s) : p.958-966 Langues : Anglais (eng) Mots-clés : attention-deficit/hyperactivity disorder  NOS1  imaging genetics  diffusion tensor imaging Index. décimale : PER Périodiques Résumé : Background The nitric oxide synthase gene (NOS1) exon 1f (ex1f) VNTR is a known genetic risk factor for Attention-Deficit/Hyperactivity Disorder (ADHD), particularly in females. NOS1 plays an important role in neurite outgrowth and may thus influence brain development, specifically white matter (WM) microstructure, which is known to be altered in ADHD. The current study aimed to investigate whether NOS1 is associated with WM microstructure in (female) individuals with and without ADHD. Methods Diffusion Tensor Imaging (DTI) scans were collected from 187 participants with ADHD (33% female) and 103 controls (50% female), aged 8–26 years, and NOS1-ex1f VNTR genotype was determined. Whole-brain analyses were conducted for fractional anisotropy (FA) and mean diffusivity (MD) to examine associations between NOS1 and WM microstructure, including possible interactions with gender and diagnosis. Results Consistent with previous literature, NOS1-ex1f was associated with total ADHD and hyperactivity-impulsivity symptoms, but not inattention; this effect was independent of gender. NOS1-ex1f was also associated with MD values in several major WM tracts in females, but not males. In females, homozygosity for the short allele was linked to higher MD values than carriership of the long allele. MD values in these regions did not correlate with ADHD symptoms. Results were similar for participants with and without ADHD. Conclusions NOS1-ex1f VNTR is associated with WM microstructure in females in a large sample of participants with ADHD and healthy controls. Whether this association is part of a neurodevelopmental pathway from NOS1 to ADHD symptoms should be further investigated in future studies. En ligne : http://dx.doi.org/10.1111/jcpp.12742 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=317 [article] Female-specific association of NOS1 genotype with white matter microstructure in ADHD patients and controls [Texte imprimé et/ou numérique] / Hanneke VAN EWIJK, Auteur ; Janita B. BRALTEN, Auteur ; Esther D. A. VAN DUIN, Auteur ; Marina HAKOBJAN, Auteur ; Jan K. BUITELAAR, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Catharina A. HARTMAN, Auteur ; Martine HOOGMAN, Auteur ; Jaap OOSTERLAAN, Auteur ; Barbara FRANKE, Auteur . - p.958-966. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 58-8 (August 2017) . - p.958-966 Mots-clés : attention-deficit/hyperactivity disorder  NOS1  imaging genetics  diffusion tensor imaging Index. décimale : PER Périodiques Résumé : Background The nitric oxide synthase gene (NOS1) exon 1f (ex1f) VNTR is a known genetic risk factor for Attention-Deficit/Hyperactivity Disorder (ADHD), particularly in females. NOS1 plays an important role in neurite outgrowth and may thus influence brain development, specifically white matter (WM) microstructure, which is known to be altered in ADHD. The current study aimed to investigate whether NOS1 is associated with WM microstructure in (female) individuals with and without ADHD. Methods Diffusion Tensor Imaging (DTI) scans were collected from 187 participants with ADHD (33% female) and 103 controls (50% female), aged 8–26 years, and NOS1-ex1f VNTR genotype was determined. Whole-brain analyses were conducted for fractional anisotropy (FA) and mean diffusivity (MD) to examine associations between NOS1 and WM microstructure, including possible interactions with gender and diagnosis. Results Consistent with previous literature, NOS1-ex1f was associated with total ADHD and hyperactivity-impulsivity symptoms, but not inattention; this effect was independent of gender. NOS1-ex1f was also associated with MD values in several major WM tracts in females, but not males. In females, homozygosity for the short allele was linked to higher MD values than carriership of the long allele. MD values in these regions did not correlate with ADHD symptoms. Results were similar for participants with and without ADHD. Conclusions NOS1-ex1f VNTR is associated with WM microstructure in females in a large sample of participants with ADHD and healthy controls. Whether this association is part of a neurodevelopmental pathway from NOS1 to ADHD symptoms should be further investigated in future studies. En ligne : http://dx.doi.org/10.1111/jcpp.12742 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=317

Potential role for immune-related genes in autism spectrum disorders: Evidence from genome-wide association meta-analysis of autistic traits / M. ARENELLA in Autism, 26-2 (February 2022)  

Public ISBD [article]  inAutism > 26-2 (February 2022) . - p.361-372 Titre : Potential role for immune-related genes in autism spectrum disorders: Evidence from genome-wide association meta-analysis of autistic traits Type de document : Texte imprimé et/ou numérique Auteurs : M. ARENELLA, Auteur ; G. CADBY, Auteur ; W. DE WITTE, Auteur ; R. M. JONES, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; E. K. MOSES, Auteur ; A. FORNITO, Auteur ; Mark A. BELLGROVE, Auteur ; Z. HAWI, Auteur ; B. JOHNSON, Auteur ; J. TIEGO, Auteur ; Jan K. BUITELAAR, Auteur ; L. A. KIEMENEY, Auteur ; G. POELMANS, Auteur ; Janita B. BRALTEN, Auteur Article en page(s) : p.361-372 Langues : Anglais (eng) Mots-clés : autism spectrum disorders  genetics  immune system  molecular and cellular biology  conflicts of interest with respect to the research, authorship and/or publication of  this article: In the past 3?years, J.K.B. has been a consultant to, member of  advisory board of and speaker for Takeda/Shire, Roche, Medice, Novartis, Angelini  and Servier. He is not an employee of any of these companies, and a stock  shareholder of any of these companies. He has no other financial or material  support, including expert testimony, patients and royalties. G.P. is the director of  Drug Target ID, Ltd. The other authors declare no conflict of interest. Index. décimale : PER Périodiques Résumé : Autism spectrum disorders are complex, with a strong genetic basis. Genetic research in autism spectrum disorders is limited by the fact that these disorders are largely heterogeneous so that patients are variable in their clinical presentations. To address this limitation, we investigated the genetics of individual dimensions of the autism spectrum disorder phenotypes, or autistic-like traits. These autistic-like traits are continuous variations in autistic behaviours that occur in the general population. Therefore, we meta-analysed data from four different population cohorts in which autistic-like traits were measured. We performed a set of genetic analyses to identify common variants for autistic-like traits, understand how these variants related to autism spectrum disorders, and how they contribute to neurobiological processes. Our results showed genetic associations with specific autistic-like traits and a link to the immune system. We offer an example of the potential to use a dimensional approach when dealing with heterogeneous, complex disorder like autism spectrum disorder. Decomposing the complex autism spectrum disorder phenotype in its core features can inform on the specific biology of these features which is likely to account to clinical variability in patients. En ligne : http://dx.doi.org/10.1177/13623613211019547 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=452 [article] Potential role for immune-related genes in autism spectrum disorders: Evidence from genome-wide association meta-analysis of autistic traits [Texte imprimé et/ou numérique] / M. ARENELLA, Auteur ; G. CADBY, Auteur ; W. DE WITTE, Auteur ; R. M. JONES, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; E. K. MOSES, Auteur ; A. FORNITO, Auteur ; Mark A. BELLGROVE, Auteur ; Z. HAWI, Auteur ; B. JOHNSON, Auteur ; J. TIEGO, Auteur ; Jan K. BUITELAAR, Auteur ; L. A. KIEMENEY, Auteur ; G. POELMANS, Auteur ; Janita B. BRALTEN, Auteur . - p.361-372. Langues : Anglais (eng) in Autism > 26-2 (February 2022) . - p.361-372 Mots-clés : autism spectrum disorders  genetics  immune system  molecular and cellular biology  conflicts of interest with respect to the research, authorship and/or publication of  this article: In the past 3?years, J.K.B. has been a consultant to, member of  advisory board of and speaker for Takeda/Shire, Roche, Medice, Novartis, Angelini  and Servier. He is not an employee of any of these companies, and a stock  shareholder of any of these companies. He has no other financial or material  support, including expert testimony, patients and royalties. G.P. is the director of  Drug Target ID, Ltd. The other authors declare no conflict of interest. Index. décimale : PER Périodiques Résumé : Autism spectrum disorders are complex, with a strong genetic basis. Genetic research in autism spectrum disorders is limited by the fact that these disorders are largely heterogeneous so that patients are variable in their clinical presentations. To address this limitation, we investigated the genetics of individual dimensions of the autism spectrum disorder phenotypes, or autistic-like traits. These autistic-like traits are continuous variations in autistic behaviours that occur in the general population. Therefore, we meta-analysed data from four different population cohorts in which autistic-like traits were measured. We performed a set of genetic analyses to identify common variants for autistic-like traits, understand how these variants related to autism spectrum disorders, and how they contribute to neurobiological processes. Our results showed genetic associations with specific autistic-like traits and a link to the immune system. We offer an example of the potential to use a dimensional approach when dealing with heterogeneous, complex disorder like autism spectrum disorder. Decomposing the complex autism spectrum disorder phenotype in its core features can inform on the specific biology of these features which is likely to account to clinical variability in patients. En ligne : http://dx.doi.org/10.1177/13623613211019547 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=452

The serotonin transporter gene polymorphism 5-HTTLPR moderates the effects of stress on attention-deficit/hyperactivity disorder / Dennis VAN DER MEER in Journal of Child Psychology and Psychiatry, 55-12 (December 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-12 (December 2014) . - p.1363-1371 Titre : The serotonin transporter gene polymorphism 5-HTTLPR moderates the effects of stress on attention-deficit/hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : Dennis VAN DER MEER, Auteur ; Catharina A. HARTMAN, Auteur ; Jennifer RICHARDS, Auteur ; Janita B. BRALTEN, Auteur ; Barbara FRANKE, Auteur ; Jaap OOSTERLAAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Stephen V. FARAONE, Auteur ; Jan K. BUITELAAR, Auteur ; Pieter J. HOEKSTRA, Auteur Article en page(s) : p.1363-1371 Langues : Anglais (eng) Mots-clés : ADHD  gene–environment interaction (GxE)  stress  serotonin transporter (5-HTTLPR) Index. décimale : PER Périodiques Résumé : Introduction The role of the serotonin transporter gene polymorphism 5-HTTLPR in attention-deficit/hyperactivity disorder (ADHD) is unclear. Heterogeneity of findings may be explained by gene–environment interactions (GxE), as it has been suggested that S-allele carriers are more reactive to psychosocial stress than L-allele homozygotes. This study aimed to investigate whether 5-HTTLPR genotype moderates the effects of stress on ADHD in a multisite prospective ADHD cohort study. Methods 5-HTTLPR genotype, as well as the number of stressful life events in the past 5 years and ongoing long-term difficulties, was determined in 671 adolescents and young adults with ADHD, their siblings, and healthy controls (57.4% male, average age 17.3 years). Linear mixed models, accounting for family relatedness, were applied to investigate the effects of genotype, experienced stress, and their interaction on ADHD severity at time point T2, while controlling for ADHD severity at T1 (mean follow-up time 5.9 years) and for comorbid internalizing problems at T2. Results The interaction between genotype and stress significantly predicted ADHD severity at T2 (p = .006), which was driven by the effect on hyperactivity–impulsivity (p = .004). Probing of the interaction effect made clear that S-allele carriers had a significantly more positive correlation between stress and ADHD severity than L-allele homozygotes. Conclusion The results show that the interaction between 5-HTTLPR and stress is a mechanism involved particularly in the hyperactivity/impulsivity dimension of ADHD, and that this is independent of comorbid internalizing problems. Further research into the neurobiological mechanisms underlying this interaction effect is warranted. En ligne : http://dx.doi.org/10.1111/jcpp.12240 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=243 [article] The serotonin transporter gene polymorphism 5-HTTLPR moderates the effects of stress on attention-deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / Dennis VAN DER MEER, Auteur ; Catharina A. HARTMAN, Auteur ; Jennifer RICHARDS, Auteur ; Janita B. BRALTEN, Auteur ; Barbara FRANKE, Auteur ; Jaap OOSTERLAAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Stephen V. FARAONE, Auteur ; Jan K. BUITELAAR, Auteur ; Pieter J. HOEKSTRA, Auteur . - p.1363-1371. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 55-12 (December 2014) . - p.1363-1371 Mots-clés : ADHD  gene–environment interaction (GxE)  stress  serotonin transporter (5-HTTLPR) Index. décimale : PER Périodiques Résumé : Introduction The role of the serotonin transporter gene polymorphism 5-HTTLPR in attention-deficit/hyperactivity disorder (ADHD) is unclear. Heterogeneity of findings may be explained by gene–environment interactions (GxE), as it has been suggested that S-allele carriers are more reactive to psychosocial stress than L-allele homozygotes. This study aimed to investigate whether 5-HTTLPR genotype moderates the effects of stress on ADHD in a multisite prospective ADHD cohort study. Methods 5-HTTLPR genotype, as well as the number of stressful life events in the past 5 years and ongoing long-term difficulties, was determined in 671 adolescents and young adults with ADHD, their siblings, and healthy controls (57.4% male, average age 17.3 years). Linear mixed models, accounting for family relatedness, were applied to investigate the effects of genotype, experienced stress, and their interaction on ADHD severity at time point T2, while controlling for ADHD severity at T1 (mean follow-up time 5.9 years) and for comorbid internalizing problems at T2. Results The interaction between genotype and stress significantly predicted ADHD severity at T2 (p = .006), which was driven by the effect on hyperactivity–impulsivity (p = .004). Probing of the interaction effect made clear that S-allele carriers had a significantly more positive correlation between stress and ADHD severity than L-allele homozygotes. Conclusion The results show that the interaction between 5-HTTLPR and stress is a mechanism involved particularly in the hyperactivity/impulsivity dimension of ADHD, and that this is independent of comorbid internalizing problems. Further research into the neurobiological mechanisms underlying this interaction effect is warranted. En ligne : http://dx.doi.org/10.1111/jcpp.12240 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=243

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