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Identifying loci for the overlap between attention-deficit/hyperactivity disorder and autism spectrum disorder using a genome-wide QTL linkage approach

Judith S Nijmeijer, Alejandro Arias-Vasquez, Nanda NJ Rommelse, Marieke E Altink, Richard JL Anney, Philip Asherson, Tobias Banaschewski, Cathelijne JM Buschgens, Ellen A Fliers, Michael Gill, et al. (2010) JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY. 49(7). p.675-685
abstract
Objective: The genetic basis for autism spectrum disorder (ASD) symptoms in children with attention-deficit/hyperactivity disorder (ADHD) was addressed using a genome-wide linkage approach. Method: Participants of the International Multi-Center ADHD Genetics study comprising 1,143 probands with ADHD and 1,453 siblings were analyzed. The total and subscale scores of the Social Communication Questionnaire (SCQ) were used as quantitative traits for multipoint regression-based linkage analyses on 5,407 autosomal single-nucleotide polymorphisms applying MERLIN-regress software, both without and with inclusion of ADHD symptom scores as covariates. Results: The analyses without ADHD symptom scores as covariates resulted in three suggestive linkage signals, i.e., on chromosomes 15q24, 16p13, and 18p11. Inclusion of ADHD symptom scores as covariates resulted in additional suggestive loci on chromosomes 7q36 and 12q24, whereas the LOD score of the locus on chromosome 15q decreased below the threshold for suggestive linkage. The loci on 7q, 16p, and 18p were found for the SCQ restricted and repetitive subscale, that on 15q was found for the SCQ communication subscale, and that on 12q for the SCQ total score. Conclusions: Our findings suggest that QTLs identified in this study are ASD specific, although the 15q QTL potentially has pleiotropic effects for ADHD and ASD. This study confirms that genetic factors influence ASD traits along a continuum of severity, as loci potentially underlying ASD symptoms in children with ADHD were identified even though subjects with autism had been excluded from the IMAGE sample, and supports the hypothesis that differential genetic factors underlie the three ASD dimensions. J. Am. Acad. Child Adolesc. Psychiatry, 2010;49(7):675-685.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
keyword
SUSCEPTIBILITY LOCI, GENETIC INFLUENCES, HOMEOBOX-TRANSCRIPTION-FACTOR, PERVASIVE DEVELOPMENTAL DISORDERS, DEFICIT HYPERACTIVITY DISORDER, TRAITS, SCAN, TWIN SAMPLE, SOCIAL-BEHAVIOR, GENERAL-POPULATION
journal title
JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
J. Am. Acad. Child Adolesc. Psychiatr.
volume
49
issue
7
pages
675 - 685
Web of Science type
Article
Web of Science id
000279276200006
JCR category
PEDIATRICS
JCR impact factor
5.148 (2010)
JCR rank
2/105 (2010)
JCR quartile
1 (2010)
ISSN
0890-8567
DOI
10.1016/j.jaac.2010.03.015
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1107409
handle
http://hdl.handle.net/1854/LU-1107409
date created
2011-01-21 12:31:37
date last changed
2016-12-19 15:46:34
@article{1107409,
  abstract     = {Objective: The genetic basis for autism spectrum disorder (ASD) symptoms in children with attention-deficit/hyperactivity disorder (ADHD) was addressed using a genome-wide linkage approach. Method: Participants of the International Multi-Center ADHD Genetics study comprising 1,143 probands with ADHD and 1,453 siblings were analyzed. The total and subscale scores of the Social Communication Questionnaire (SCQ) were used as quantitative traits for multipoint regression-based linkage analyses on 5,407 autosomal single-nucleotide polymorphisms applying MERLIN-regress software, both without and with inclusion of ADHD symptom scores as covariates. Results: The analyses without ADHD symptom scores as covariates resulted in three suggestive linkage signals, i.e., on chromosomes 15q24, 16p13, and 18p11. Inclusion of ADHD symptom scores as covariates resulted in additional suggestive loci on chromosomes 7q36 and 12q24, whereas the LOD score of the locus on chromosome 15q decreased below the threshold for suggestive linkage. The loci on 7q, 16p, and 18p were found for the SCQ restricted and repetitive subscale, that on 15q was found for the SCQ communication subscale, and that on 12q for the SCQ total score. Conclusions: Our findings suggest that QTLs identified in this study are ASD specific, although the 15q QTL potentially has pleiotropic effects for ADHD and ASD. This study confirms that genetic factors influence ASD traits along a continuum of severity, as loci potentially underlying ASD symptoms in children with ADHD were identified even though subjects with autism had been excluded from the IMAGE sample, and supports the hypothesis that differential genetic factors underlie the three ASD dimensions. J. Am. Acad. Child Adolesc. Psychiatry, 2010;49(7):675-685.},
  author       = {Nijmeijer, Judith S and Arias-Vasquez, Alejandro and Rommelse, Nanda NJ and Altink, Marieke E and Anney, Richard JL and Asherson, Philip and Banaschewski, Tobias and Buschgens, Cathelijne JM and Fliers, Ellen A and Gill, Michael and Minderaa, Ruud B and Poustka, Luise and Sergeant, Joseph A and Buitelaar, Jan K and Franke, Barbara and Ebstein, Richard P and Miranda, Ana and Mulas, Fernando and Oades, Robert D and Roeyers, Herbert and Rothenberger, Aribert and Barke, Edmund and Steinhausen, Hans-Christoph and Faraone, Stephen V and Hartman, Catharina A and Hoekstra, Pieter J},
  issn         = {0890-8567},
  journal      = {JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY},
  keyword      = {SUSCEPTIBILITY LOCI,GENETIC INFLUENCES,HOMEOBOX-TRANSCRIPTION-FACTOR,PERVASIVE DEVELOPMENTAL DISORDERS,DEFICIT HYPERACTIVITY DISORDER,TRAITS,SCAN,TWIN SAMPLE,SOCIAL-BEHAVIOR,GENERAL-POPULATION},
  language     = {eng},
  number       = {7},
  pages        = {675--685},
  title        = {Identifying loci for the overlap between attention-deficit/hyperactivity disorder and autism spectrum disorder using a genome-wide QTL linkage approach},
  url          = {http://dx.doi.org/10.1016/j.jaac.2010.03.015},
  volume       = {49},
  year         = {2010},
}

Chicago
Nijmeijer, Judith S, Alejandro Arias-Vasquez, Nanda NJ Rommelse, Marieke E Altink, Richard JL Anney, Philip Asherson, Tobias Banaschewski, et al. 2010. “Identifying Loci for the Overlap Between Attention-deficit/hyperactivity Disorder and Autism Spectrum Disorder Using a Genome-wide QTL Linkage Approach.” JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY 49 (7): 675–685.
APA
Nijmeijer, J. S., Arias-Vasquez, A., Rommelse, N. N., Altink, M. E., Anney, R. J., Asherson, P., Banaschewski, T., et al. (2010). Identifying loci for the overlap between attention-deficit/hyperactivity disorder and autism spectrum disorder using a genome-wide QTL linkage approach. JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY, 49(7), 675–685.
Vancouver
1.
Nijmeijer JS, Arias-Vasquez A, Rommelse NN, Altink ME, Anney RJ, Asherson P, et al. Identifying loci for the overlap between attention-deficit/hyperactivity disorder and autism spectrum disorder using a genome-wide QTL linkage approach. JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY. 2010;49(7):675–85.
MLA
Nijmeijer, Judith S, Alejandro Arias-Vasquez, Nanda NJ Rommelse, et al. “Identifying Loci for the Overlap Between Attention-deficit/hyperactivity Disorder and Autism Spectrum Disorder Using a Genome-wide QTL Linkage Approach.” JOURNAL OF THe AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY 49.7 (2010): 675–685. Print.