Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: genome-wide association study of both common and rare variants. Yang, L., Neale, B. M, Liu, L., Lee, S H., Wray, N. R, Ji, N., Li, H., Qian, Q., Wang, D., Li, J., Faraone, S. V, Wang, Y., Doyle, A. E, Reif, A., Rothenberger, A., Franke, B., Sonuga-Barke, E. J S, Steinhausen, H., Buitelaar, J. K, Kuntsi, J., Biederman, J., Lesch, K., Kent, L., Asherson, P., Oades, R. D, Loo, S. K, Nelson, S. F, Smalley, S. L, Banaschewski, T., Arias Vasquez, A., Todorov, A., Charach, A., Miranda, A., Warnke, A., Thapar, A., Cormand, B., Freitag, C., Mick, E., Mulas, F., Middleton, F., HakonarsonHakonarson, H., Palmason, H., Schäfer, H., Roeyers, H., McGough, J. J, Romanos, J., Crosbie, J., Meyer, J., Ramos-Quiroga, J. A., Sergeant, J., Elia, J., Langely, K., Nisenbaum, L., Romanos, M., Daly, M. J, Ribasés, M., Gill, M., O'Donovan, M., Owen, M., Casas, M., Bayés, M., Lambregts-Rommelse, N., Williams, N., Holmans, P., Anney, R. J L, Ebstein, R. P, Schachar, R., Medland, S. E, Ripke, S., Walitza, S., Nguyen, T. T., Renner, T. J, & Hu, X. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 162B(5):419–30, July, 2013. ![Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: genome-wide association study of both common and rare variants. [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Attention-deficit hyperactivity disorder (ADHD) is a complex polygenic disorder. This study aimed to discover common and rare DNA variants associated with ADHD in a large homogeneous Han Chinese ADHD case-control sample. The sample comprised 1,040 cases and 963 controls. All cases met DSM-IV ADHD diagnostic criteria. We used the Affymetrix6.0 array to assay both single nucleotide polymorphisms (SNPs) and copy number variants (CNVs). Genome-wide association analyses were performed using PLINK. SNP-heritability and SNP-genetic correlations with ADHD in Caucasians were estimated with genome-wide complex trait analysis (GCTA). Pathway analyses were performed using the Interval enRICHment Test (INRICH), the Disease Association Protein-Protein Link Evaluator (DAPPLE), and the Genomic Regions Enrichment of Annotations Tool (GREAT). We did not find genome-wide significance for single SNPs but did find an increased burden of large, rare CNVs in the ADHD sample (P = 0.038). SNP-heritability was estimated to be 0.42 (standard error, 0.13, P = 0.0017) and the SNP-genetic correlation with European Ancestry ADHD samples was 0.39 (SE 0.15, P = 0.0072). The INRICH, DAPPLE, and GREAT analyses implicated several gene ontology cellular components, including neuron projections and synaptic components, which are consistent with a neurodevelopmental pathophysiology for ADHD. This study suggested the genetic architecture of ADHD comprises both common and rare variants. Some common causal variants are likely to be shared between Han Chinese and Caucasians. Complex neurodevelopmental networks may underlie ADHD's etiology.
@article{yang_polygenic_2013,
title = {Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: genome-wide association study of both common and rare variants.},
volume = {162B},
issn = {1552-485X},
url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4321789&tool=pmcentrez&rendertype=abstract},
doi = {10.1002/ajmg.b.32169},
abstract = {Attention-deficit hyperactivity disorder (ADHD) is a complex polygenic disorder. This study aimed to discover common and rare DNA variants associated with ADHD in a large homogeneous Han Chinese ADHD case-control sample. The sample comprised 1,040 cases and 963 controls. All cases met DSM-IV ADHD diagnostic criteria. We used the Affymetrix6.0 array to assay both single nucleotide polymorphisms (SNPs) and copy number variants (CNVs). Genome-wide association analyses were performed using PLINK. SNP-heritability and SNP-genetic correlations with ADHD in Caucasians were estimated with genome-wide complex trait analysis (GCTA). Pathway analyses were performed using the Interval enRICHment Test (INRICH), the Disease Association Protein-Protein Link Evaluator (DAPPLE), and the Genomic Regions Enrichment of Annotations Tool (GREAT). We did not find genome-wide significance for single SNPs but did find an increased burden of large, rare CNVs in the ADHD sample (P = 0.038). SNP-heritability was estimated to be 0.42 (standard error, 0.13, P = 0.0017) and the SNP-genetic correlation with European Ancestry ADHD samples was 0.39 (SE 0.15, P = 0.0072). The INRICH, DAPPLE, and GREAT analyses implicated several gene ontology cellular components, including neuron projections and synaptic components, which are consistent with a neurodevelopmental pathophysiology for ADHD. This study suggested the genetic architecture of ADHD comprises both common and rare variants. Some common causal variants are likely to be shared between Han Chinese and Caucasians. Complex neurodevelopmental networks may underlie ADHD's etiology.},
number = {5},
urldate = {2015-04-13},
journal = {American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics},
author = {Yang, Li and Neale, Benjamin M and Liu, Lu and Lee, S Hong and Wray, Naomi R and Ji, Ning and Li, Haimei and Qian, Qiujin and Wang, Dongliang and Li, Jun and Faraone, Stephen V and Wang, Yufeng and Doyle, Alysa E and Reif, Andreas and Rothenberger, Aribert and Franke, Barbara and Sonuga-Barke, Edmund J S and Steinhausen, Hans-Christoph and Buitelaar, Jan K and Kuntsi, Jonna and Biederman, Joseph and Lesch, Klaus-Peter and Kent, Lindsey and Asherson, Philip and Oades, Robert D and Loo, Sandra K and Nelson, Stan F and Smalley, Susan L and Banaschewski, Tobias and Arias Vasquez, Alejandro and Todorov, Alexandre and Charach, Alice and Miranda, Ana and Warnke, Andreas and Thapar, Anita and Cormand, Bru and Freitag, Christine and Mick, Eric and Mulas, Fernando and Middleton, Frank and HakonarsonHakonarson, Hakon and Palmason, Haukur and Schäfer, Helmut and Roeyers, Herbert and McGough, James J and Romanos, Jasmin and Crosbie, Jennifer and Meyer, Jobst and Ramos-Quiroga, Josep Antoni and Sergeant, Joseph and Elia, Josephine and Langely, Kate and Nisenbaum, Laura and Romanos, Marcel and Daly, Mark J and Ribasés, Marta and Gill, Michael and O'Donovan, Michael and Owen, Michael and Casas, Miguel and Bayés, Mònica and Lambregts-Rommelse, Nanda and Williams, Nigel and Holmans, Peter and Anney, Richard J L and Ebstein, Richard P and Schachar, Russell and Medland, Sarah E and Ripke, Stephan and Walitza, Susanne and Nguyen, Thuy Trang and Renner, Tobias J and Hu, Xiaolan},
month = jul,
year = {2013},
pmid = {23728934},
keywords = {Adolescent, Attention Deficit Disorder with Hyperactivity, Attention Deficit Disorder with Hyperactivity: gen, Case-Control Studies, Child, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide},
pages = {419--30},
}
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Attention Deficit Disorder with Hyperactivity, Attention Deficit Disorder with Hyperactivity: gen, Case-Control Studies, Child, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide","pages":"419–30","bibtex":"@article{yang_polygenic_2013,\n\ttitle = {Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: genome-wide association study of both common and rare variants.},\n\tvolume = {162B},\n\tissn = {1552-485X},\n\turl = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4321789&tool=pmcentrez&rendertype=abstract},\n\tdoi = {10.1002/ajmg.b.32169},\n\tabstract = {Attention-deficit hyperactivity disorder (ADHD) is a complex polygenic disorder. This study aimed to discover common and rare DNA variants associated with ADHD in a large homogeneous Han Chinese ADHD case-control sample. The sample comprised 1,040 cases and 963 controls. All cases met DSM-IV ADHD diagnostic criteria. We used the Affymetrix6.0 array to assay both single nucleotide polymorphisms (SNPs) and copy number variants (CNVs). Genome-wide association analyses were performed using PLINK. SNP-heritability and SNP-genetic correlations with ADHD in Caucasians were estimated with genome-wide complex trait analysis (GCTA). Pathway analyses were performed using the Interval enRICHment Test (INRICH), the Disease Association Protein-Protein Link Evaluator (DAPPLE), and the Genomic Regions Enrichment of Annotations Tool (GREAT). We did not find genome-wide significance for single SNPs but did find an increased burden of large, rare CNVs in the ADHD sample (P = 0.038). SNP-heritability was estimated to be 0.42 (standard error, 0.13, P = 0.0017) and the SNP-genetic correlation with European Ancestry ADHD samples was 0.39 (SE 0.15, P = 0.0072). The INRICH, DAPPLE, and GREAT analyses implicated several gene ontology cellular components, including neuron projections and synaptic components, which are consistent with a neurodevelopmental pathophysiology for ADHD. This study suggested the genetic architecture of ADHD comprises both common and rare variants. Some common causal variants are likely to be shared between Han Chinese and Caucasians. Complex neurodevelopmental networks may underlie ADHD's etiology.},\n\tnumber = {5},\n\turldate = {2015-04-13},\n\tjournal = {American journal of medical genetics. 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