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      Polymorphisms in the oxytocin receptor gene are associated with the development of psychopathy.

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          Abstract

          The co-occurrence of child conduct problems (CPs) and callous-unemotional (CU) traits confers risk for psychopathy. The oxytocin (OXT) system is a likely candidate for involvement in the development of psychopathy. We tested variations in the OXT receptor gene (OXTR) in CP children and adolescents with varying levels of CU traits. Two samples of Caucasian children, aged 4-16 years, who met DSM criteria for disruptive behavior problems and had no features of autism spectrum disorder, were stratified into low versus high CU traits. Measures were the frequencies of nine candidate OXTR polymorphisms (single nucleotide polymorphisms). In Sample 1, high CU traits were associated with single nucleotide polymorphism rs1042778 in the 3' untranslated region of OXTR and the CGCT haplotype of rs2268490, rs2254298, rs237889, and rs13316193. The association of rs1042778 was replicated in the second rural sample and held across gender and child versus adolescent age groups. We conclude that polymorphic variation of the OXTR characterizes children with high levels of CU traits and CPs. The results are consistent with a hypothesized role of OXT in the developmental antecedents of psychopathy, particularly the differential amygdala activation model of psychopathic traits, and add genetic evidence that high CU traits specify a distinct subgroup within CP children.

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          Author and article information

          Journal
          Dev. Psychopathol.
          Development and psychopathology
          1469-2198
          0954-5794
          Feb 2014
          : 26
          : 1
          Affiliations
          [1 ] University of New South Wales.
          [2 ] University of Sydney.
          [3 ] Sydney Children's Hospital.
          [4 ] Children's Hospital at Westmead.
          [5 ] National University of Singapore.
          Article
          S0954579413000485
          10.1017/S0954579413000485
          24059750
          b94ee7b4-2512-4612-a10f-cbf0c39c674d
          History

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