Case-Control Study of Six Genes Asymmetrically Expressed in the Two Cerebral Hemispheres

Association of BAIAP2 with Attention-Deficit/Hyperactivity Disorder

Marta Ribasés, Rosa Bosch, Amaia Hervás, Josep Antoni Ramos-Quiroga, Cristina Sánchez-Mora, Anna Bielsa, Xavier Gastaminza, Sílvia Guijarro-Domingo, Mariana Nogueira, Núria Gómez-Barros, Susanne Kreiker, Silke Groß-Lesch, Christian P. Jacob, Klaus Peter Lesch, Andreas Reif, Stefan Johansson, Kerstin J. Plessen, Per M. Knappskog, Jan Haavik, Xavier P. Estivill & 3 others Miguel Casas, Mònica Bayés, Bru Cormand

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Background: Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset neuropsychiatric disease that persists into adulthood in at least 30% of patients. There is evidence suggesting that abnormal left-right brain asymmetries in ADHD patients may be involved in a variety of ADHD-related cognitive processes, including sustained attention, working memory, response inhibition and planning. Although mechanisms underlying cerebral lateralization are unknown, left-right cortical asymmetry has been associated with transcriptional asymmetry at embryonic stages and several genes differentially expressed between hemispheres have been identified. Methods: We selected six functional candidate genes showing at least 1.9-fold differential expression between hemispheres (BAIAP2, DAPPER1, LMO4, NEUROD6, ATP2B3, and ID2) and performed a case-control association study in an initial Spanish sample of 587 ADHD patients (270 adults and 317 children) and 587 control subjects. Results: The single- and multiple-marker analysis provided evidence for a contribution of BAIAP2 to adulthood ADHD (p = .0026 and p = .0016, respectively). We thus tested BAIAP2 for replication in two independent adult samples from Germany (639 ADHD patients and 612 control subjects) and Norway (417 ADHD cases and 469 control subjects). While no significant results were observed in the Norwegian sample, we replicated the initial association between BAIAP2 and adulthood ADHD in the German population (p = .0062). Conclusions: Our results support the participation of BAIAP2 in the continuity of ADHD across life span, at least in some of the populations analyzed, and suggest that genetic factors potentially influencing abnormal cerebral lateralization may be involved in this disorder.

Original languageEnglish
Pages (from-to)926-934
Number of pages9
JournalBiological Psychiatry
Volume66
Issue number10
DOIs
Publication statusPublished - 15 Nov 2009
Externally publishedYes

Fingerprint

Cerebrum
Attention Deficit Disorder with Hyperactivity
Case-Control Studies
Genes
Norway
Short-Term Memory
Population
Germany
Brain

Keywords

  • ADHD
  • attention-deficit hyperactivity disorder
  • BAIAP2
  • brain asymmetry
  • case-control association study

ASJC Scopus subject areas

  • Biological Psychiatry

Cite this

Case-Control Study of Six Genes Asymmetrically Expressed in the Two Cerebral Hemispheres : Association of BAIAP2 with Attention-Deficit/Hyperactivity Disorder. / Ribasés, Marta; Bosch, Rosa; Hervás, Amaia; Ramos-Quiroga, Josep Antoni; Sánchez-Mora, Cristina; Bielsa, Anna; Gastaminza, Xavier; Guijarro-Domingo, Sílvia; Nogueira, Mariana; Gómez-Barros, Núria; Kreiker, Susanne; Groß-Lesch, Silke; Jacob, Christian P.; Lesch, Klaus Peter; Reif, Andreas; Johansson, Stefan; Plessen, Kerstin J.; Knappskog, Per M.; Haavik, Jan; Estivill, Xavier P.; Casas, Miguel; Bayés, Mònica; Cormand, Bru.

In: Biological Psychiatry, Vol. 66, No. 10, 15.11.2009, p. 926-934.

Research output: Contribution to journalArticle

Ribasés, M, Bosch, R, Hervás, A, Ramos-Quiroga, JA, Sánchez-Mora, C, Bielsa, A, Gastaminza, X, Guijarro-Domingo, S, Nogueira, M, Gómez-Barros, N, Kreiker, S, Groß-Lesch, S, Jacob, CP, Lesch, KP, Reif, A, Johansson, S, Plessen, KJ, Knappskog, PM, Haavik, J, Estivill, XP, Casas, M, Bayés, M & Cormand, B 2009, 'Case-Control Study of Six Genes Asymmetrically Expressed in the Two Cerebral Hemispheres: Association of BAIAP2 with Attention-Deficit/Hyperactivity Disorder', Biological Psychiatry, vol. 66, no. 10, pp. 926-934. https://doi.org/10.1016/j.biopsych.2009.06.024
Ribasés, Marta ; Bosch, Rosa ; Hervás, Amaia ; Ramos-Quiroga, Josep Antoni ; Sánchez-Mora, Cristina ; Bielsa, Anna ; Gastaminza, Xavier ; Guijarro-Domingo, Sílvia ; Nogueira, Mariana ; Gómez-Barros, Núria ; Kreiker, Susanne ; Groß-Lesch, Silke ; Jacob, Christian P. ; Lesch, Klaus Peter ; Reif, Andreas ; Johansson, Stefan ; Plessen, Kerstin J. ; Knappskog, Per M. ; Haavik, Jan ; Estivill, Xavier P. ; Casas, Miguel ; Bayés, Mònica ; Cormand, Bru. / Case-Control Study of Six Genes Asymmetrically Expressed in the Two Cerebral Hemispheres : Association of BAIAP2 with Attention-Deficit/Hyperactivity Disorder. In: Biological Psychiatry. 2009 ; Vol. 66, No. 10. pp. 926-934.
@article{e920aba998aa431f9c70bbed85da527f,
title = "Case-Control Study of Six Genes Asymmetrically Expressed in the Two Cerebral Hemispheres: Association of BAIAP2 with Attention-Deficit/Hyperactivity Disorder",
abstract = "Background: Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset neuropsychiatric disease that persists into adulthood in at least 30{\%} of patients. There is evidence suggesting that abnormal left-right brain asymmetries in ADHD patients may be involved in a variety of ADHD-related cognitive processes, including sustained attention, working memory, response inhibition and planning. Although mechanisms underlying cerebral lateralization are unknown, left-right cortical asymmetry has been associated with transcriptional asymmetry at embryonic stages and several genes differentially expressed between hemispheres have been identified. Methods: We selected six functional candidate genes showing at least 1.9-fold differential expression between hemispheres (BAIAP2, DAPPER1, LMO4, NEUROD6, ATP2B3, and ID2) and performed a case-control association study in an initial Spanish sample of 587 ADHD patients (270 adults and 317 children) and 587 control subjects. Results: The single- and multiple-marker analysis provided evidence for a contribution of BAIAP2 to adulthood ADHD (p = .0026 and p = .0016, respectively). We thus tested BAIAP2 for replication in two independent adult samples from Germany (639 ADHD patients and 612 control subjects) and Norway (417 ADHD cases and 469 control subjects). While no significant results were observed in the Norwegian sample, we replicated the initial association between BAIAP2 and adulthood ADHD in the German population (p = .0062). Conclusions: Our results support the participation of BAIAP2 in the continuity of ADHD across life span, at least in some of the populations analyzed, and suggest that genetic factors potentially influencing abnormal cerebral lateralization may be involved in this disorder.",
keywords = "ADHD, attention-deficit hyperactivity disorder, BAIAP2, brain asymmetry, case-control association study",
author = "Marta Ribas{\'e}s and Rosa Bosch and Amaia Herv{\'a}s and Ramos-Quiroga, {Josep Antoni} and Cristina S{\'a}nchez-Mora and Anna Bielsa and Xavier Gastaminza and S{\'i}lvia Guijarro-Domingo and Mariana Nogueira and N{\'u}ria G{\'o}mez-Barros and Susanne Kreiker and Silke Gro{\ss}-Lesch and Jacob, {Christian P.} and Lesch, {Klaus Peter} and Andreas Reif and Stefan Johansson and Plessen, {Kerstin J.} and Knappskog, {Per M.} and Jan Haavik and Estivill, {Xavier P.} and Miguel Casas and M{\`o}nica Bay{\'e}s and Bru Cormand",
year = "2009",
month = "11",
day = "15",
doi = "10.1016/j.biopsych.2009.06.024",
language = "English",
volume = "66",
pages = "926--934",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier USA",
number = "10",

}

TY - JOUR

T1 - Case-Control Study of Six Genes Asymmetrically Expressed in the Two Cerebral Hemispheres

T2 - Association of BAIAP2 with Attention-Deficit/Hyperactivity Disorder

AU - Ribasés, Marta

AU - Bosch, Rosa

AU - Hervás, Amaia

AU - Ramos-Quiroga, Josep Antoni

AU - Sánchez-Mora, Cristina

AU - Bielsa, Anna

AU - Gastaminza, Xavier

AU - Guijarro-Domingo, Sílvia

AU - Nogueira, Mariana

AU - Gómez-Barros, Núria

AU - Kreiker, Susanne

AU - Groß-Lesch, Silke

AU - Jacob, Christian P.

AU - Lesch, Klaus Peter

AU - Reif, Andreas

AU - Johansson, Stefan

AU - Plessen, Kerstin J.

AU - Knappskog, Per M.

AU - Haavik, Jan

AU - Estivill, Xavier P.

AU - Casas, Miguel

AU - Bayés, Mònica

AU - Cormand, Bru

PY - 2009/11/15

Y1 - 2009/11/15

N2 - Background: Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset neuropsychiatric disease that persists into adulthood in at least 30% of patients. There is evidence suggesting that abnormal left-right brain asymmetries in ADHD patients may be involved in a variety of ADHD-related cognitive processes, including sustained attention, working memory, response inhibition and planning. Although mechanisms underlying cerebral lateralization are unknown, left-right cortical asymmetry has been associated with transcriptional asymmetry at embryonic stages and several genes differentially expressed between hemispheres have been identified. Methods: We selected six functional candidate genes showing at least 1.9-fold differential expression between hemispheres (BAIAP2, DAPPER1, LMO4, NEUROD6, ATP2B3, and ID2) and performed a case-control association study in an initial Spanish sample of 587 ADHD patients (270 adults and 317 children) and 587 control subjects. Results: The single- and multiple-marker analysis provided evidence for a contribution of BAIAP2 to adulthood ADHD (p = .0026 and p = .0016, respectively). We thus tested BAIAP2 for replication in two independent adult samples from Germany (639 ADHD patients and 612 control subjects) and Norway (417 ADHD cases and 469 control subjects). While no significant results were observed in the Norwegian sample, we replicated the initial association between BAIAP2 and adulthood ADHD in the German population (p = .0062). Conclusions: Our results support the participation of BAIAP2 in the continuity of ADHD across life span, at least in some of the populations analyzed, and suggest that genetic factors potentially influencing abnormal cerebral lateralization may be involved in this disorder.

AB - Background: Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset neuropsychiatric disease that persists into adulthood in at least 30% of patients. There is evidence suggesting that abnormal left-right brain asymmetries in ADHD patients may be involved in a variety of ADHD-related cognitive processes, including sustained attention, working memory, response inhibition and planning. Although mechanisms underlying cerebral lateralization are unknown, left-right cortical asymmetry has been associated with transcriptional asymmetry at embryonic stages and several genes differentially expressed between hemispheres have been identified. Methods: We selected six functional candidate genes showing at least 1.9-fold differential expression between hemispheres (BAIAP2, DAPPER1, LMO4, NEUROD6, ATP2B3, and ID2) and performed a case-control association study in an initial Spanish sample of 587 ADHD patients (270 adults and 317 children) and 587 control subjects. Results: The single- and multiple-marker analysis provided evidence for a contribution of BAIAP2 to adulthood ADHD (p = .0026 and p = .0016, respectively). We thus tested BAIAP2 for replication in two independent adult samples from Germany (639 ADHD patients and 612 control subjects) and Norway (417 ADHD cases and 469 control subjects). While no significant results were observed in the Norwegian sample, we replicated the initial association between BAIAP2 and adulthood ADHD in the German population (p = .0062). Conclusions: Our results support the participation of BAIAP2 in the continuity of ADHD across life span, at least in some of the populations analyzed, and suggest that genetic factors potentially influencing abnormal cerebral lateralization may be involved in this disorder.

KW - ADHD

KW - attention-deficit hyperactivity disorder

KW - BAIAP2

KW - brain asymmetry

KW - case-control association study

UR - http://www.scopus.com/inward/record.url?scp=70350568296&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70350568296&partnerID=8YFLogxK

U2 - 10.1016/j.biopsych.2009.06.024

DO - 10.1016/j.biopsych.2009.06.024

M3 - Article

VL - 66

SP - 926

EP - 934

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

IS - 10

ER -