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      Deviant Peer Affiliation and Antisocial Behavior: Interaction with Monoamine Oxidase A (MAOA) Genotype

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          Abstract

          Although genetic and environmental factors are separately implicated in the development of antisocial behavior (ASB), interactive models have emerged relatively recently, particularly those incorporating molecular genetic data. Using a large sample of male Caucasian adolescents and young adults from the National Longitudinal Study of Adolescent Health (Add Health), the association of deviant peer affiliation, the 30-base pair variable number tandem repeat polymorphism in promoter region of the monoamine oxidase-A (MAOA) gene, and their interaction, with antisocial behavior (ASB) was investigated. Weighted analyses accounting for over-sampling and clustering within schools as well as controlling for age and wave suggested that deviant peer affiliation and MAOA genotype were each significantly associated with levels of overt ASB across a 6-year period. Only deviant peer affiliation was significantly related to covert ASB, however. Additionally, there was evidence suggestive of a gene-environment interaction (G × E) where the influence of deviant peer affiliation on overt ASB was significantly stronger among individuals with the high-activity MAOA genotype than the low-activity genotype. MAOA was not significantly associated with deviant peer affiliation, thus strengthening the inference of G × E rather than gene-environment correlation (rGE). Different forms of gene-environment interplay and implications for future research on ASB are discussed.

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          The future of genetic studies of complex human diseases.

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            A functional polymorphism in the monoamine oxidase A gene promoter.

            We describe a new polymorphism upstream of the gene for monoamine oxidase A (MAOA), an important enzyme in human physiology and behavior. The polymorphism, which is located 1.2 kb upstream of the MAOA coding sequences, consists of a 30-bp repeated sequence present in 3, 3.5, 4, or 5 copies. The polymorphism is in linkage disequilibrium with other MAOA and MAOB gene markers and displays significant variations in allele frequencies across ethnic groups. The polymorphism has been shown to affect the transcriptional activity of the MAOA gene promoter by gene fusion and transfection experiments involving three different cell types. Alleles with 3.5 or 4 copies of the repeat sequence are transcribed 2-10 times more efficiently than those with 3 or 5 copies of the repeat, suggesting an optimal length for the regulatory region. This promoter region polymorphism may be useful as both a functional and an anonymous genetic marker for MAOA.
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              Copy-number variations associated with neuropsychiatric conditions.

              Neuropsychiatric conditions such as autism and schizophrenia have long been attributed to genetic alterations, but identifying the genes responsible has proved challenging. Microarray experiments have now revealed abundant copy-number variation--a type of variation in which stretches of DNA are duplicated, deleted and sometimes rearranged--in the human population. Genes affected by copy-number variation are good candidates for research into disease susceptibility. The complexity of neuropsychiatric genetics, however, dictates that assessment of the biomedical relevance of copy-number variants and the genes that they affect needs to be considered in an integrated context.
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                Author and article information

                Contributors
                stevelee@psych.ucla.edu
                Journal
                J Abnorm Child Psychol
                Journal of Abnormal Child Psychology
                Springer US (Boston )
                0091-0627
                1573-2835
                9 December 2010
                9 December 2010
                April 2011
                : 39
                : 3
                : 321-332
                Affiliations
                Department of Psychology, University of California, Los Angeles (UCLA), 1285 Franz Hall, Box 951563, Los Angeles, CA 90095-1563 USA
                Article
                9474
                10.1007/s10802-010-9474-2
                3066389
                21152968
                59ea5465-4714-4a4e-a330-70b035b3626f
                © The Author(s) 2010
                History
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media, LLC 2011

                Clinical Psychology & Psychiatry
                deviant peer affiliation,gene–environment interaction,longitudinal,antisocial behavior

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