{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T07:23:34Z","timestamp":1769066614871,"version":"3.49.0"},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,6,19]],"date-time":"2014-06-19T00:00:00Z","timestamp":1403136000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81301171"],"award-info":[{"award-number":["81301171"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100012166","name":"National Basic Research Program of China","doi-asserted-by":"crossref","award":["2014CB846104"],"award-info":[{"award-number":["2014CB846104"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100004602","name":"Program for New Century Excellent Talents in University","doi-asserted-by":"crossref","award":["NCET-11-0013"],"award-info":[{"award-number":["NCET-11-0013"]}],"id":[{"id":"10.13039\/501100004602","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Child Psychology Psychiatry"],"published-print":{"date-parts":[[2015,1]]},"abstract":"\n Background<\/jats:title>\n \n Attention\u2010deficit\/hyperactivity disorder (\n ADHD<\/jats:styled-content>\n ) and oppositional defiant disorder (\n ODD<\/jats:styled-content>\n ) often coexist and shared some genetic influences. Evidence from the existing literature indicated that comorbid with\n ODD<\/jats:styled-content>\n may increase the heterogeneity of\n ADHD<\/jats:styled-content>\n genetics. Our present study sought to investigate the role of norepinephrine transporter gene (\n \n NET<\/jats:styled-content>\n 1\n <\/jats:italic>\n ) for\n ADHD<\/jats:styled-content>\n comorbid with\n ODD<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Six single nucleotide polymorphisms (\n SNP<\/jats:styled-content>\n s) of\n \n NET<\/jats:styled-content>\n 1\n <\/jats:italic>\n were genotyped for a total of 1,815\n ADHD<\/jats:styled-content>\n cases, including 587 subjects (32.3%) with\n ODD<\/jats:styled-content>\n . Chi\u2010square tests were conducted for pseudo case\u2013control study comparing allelic and genotypic distributions between\n ADHD<\/jats:styled-content>\n with and without\n ODD<\/jats:styled-content>\n . Among them, there were 1,249 probands together with their parents composing trios for family\u2010based association studies using transmission disequilibrium tests (\n TDT<\/jats:styled-content>\n s). In addition, 1,337\n ADHD<\/jats:styled-content>\n probands have detailed information of\n ODD<\/jats:styled-content>\n symptoms and were included for quantitative analyses with genotypes using analyses of covariance (\n ANCOVA<\/jats:styled-content>\n ). To consider the overlap and correlation of other comorbidities with\n ODD<\/jats:styled-content>\n and eliminate their potential confounding effect, we further repeated above analyses for \u2018pure\n ADHD<\/jats:styled-content>\n +\n ODD<\/jats:styled-content>\n \u2019 versus \u2018\n ADHD<\/jats:styled-content>\n \u2010only\u2019 after excluding other comorbidities except for\n ODD<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The pseudo case\u2013control study showed different allelic and genotypic distributions of\n SNP<\/jats:styled-content>\n rs3785143 between\n ADHD<\/jats:styled-content>\n with\n ODD<\/jats:styled-content>\n and those without\n ODD<\/jats:styled-content>\n . Family\u2010based association tests indicated overtransmission of the T allele of rs3785143 in\n ADHD<\/jats:styled-content>\n with\n ODD<\/jats:styled-content>\n trios, but no biased transmission in those without\n ODD<\/jats:styled-content>\n .\n ANCOVA<\/jats:styled-content>\n showed association between genotypes of rs3785143 with\n ODD<\/jats:styled-content>\n symptoms in\n ADHD<\/jats:styled-content>\n probands, especially with \u2018Argumentative\/Defiant Behavior (\n ADB<\/jats:styled-content>\n )\u2019 dimension after controlling gender, age, clinical subtypes and intelligence. Above association still existed after removing the samples with other comorbidities.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n \n NET<\/jats:styled-content>\n 1\n <\/jats:italic>\n was associated with comorbidity of\n ODD<\/jats:styled-content>\n and\n ODD<\/jats:styled-content>\n symptoms in\n ADHD<\/jats:styled-content>\n probands. Our findings emphasize the importance of considering the comorbidity of\n ODD<\/jats:styled-content>\n in\n ADHD<\/jats:styled-content>\n genetic studies, especially\n ADHD<\/jats:styled-content>\n with\n ADB<\/jats:styled-content>\n . However, further replication in independent sample or different populations is still needed.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/jcpp.12278","type":"journal-article","created":{"date-parts":[[2014,6,19]],"date-time":"2014-06-19T06:34:01Z","timestamp":1403159641000},"page":"58-66","source":"Crossref","is-referenced-by-count":17,"title":["The possible involvement of genetic variants of\n \n NET<\/scp>\n 1\n <\/i>\n in the etiology of attention\u2010deficit\/hyperactivity disorder comorbid with oppositional defiant disorder"],"prefix":"10.1111","volume":"56","author":[{"given":"Lu","family":"Liu","sequence":"first","affiliation":[{"name":"Peking University Sixth Hospital Institute of Mental Health Beijing China"},{"name":"Key Laboratory of Mental Health Ministry of Health (Peking University) Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jia","family":"Cheng","sequence":"additional","affiliation":[{"name":"Peking University Sixth Hospital Institute 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