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      Trauma, genes, and the neurobiology of personality disorders.

      1 , ,
      Annals of the New York Academy of Sciences
      Wiley

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          Abstract

          A model for personality dysfunction posits an interaction between inherited susceptibility and environmental factors such as childhood trauma. Core biological vulnerabilities in personality include dimensions of affective instability, impulsive aggression, and cognition/perceptual domains. For the dimension of impulsive aggression, often seen in borderline personality disorder (BPD), the underlying neurobiology involves deficits in central serotonin function and alterations in specific brain regions in the cingulate and the medial and orbital prefrontal cortex. The role of trauma in the development of personality disorder and especially for BPD remains unclear. Although recent studies suggest that BPD is not a trauma-spectrum disorder and that it is biologically distinct from posttraumatic stress disorder, high rates of childhood abuse and neglect do exist for individuals with personality dysfunction. Personality symptom clusters seem to be unrelated to specific abuses, but they may relate to more enduring aspects of interpersonal and family environments in childhood. Whereas twin and family studies indicate a partially heritable basis for impulsive aggression, studies of serotonin-related genes to date suggest only modest contributions to behavior. Gene-environment interactions involving childhood maltreatment are demonstrated in recent studies on antisocial behaviors and aggressive rhesus monkeys and highlight the need for further research in this important area.

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          Author and article information

          Journal
          Ann N Y Acad Sci
          Annals of the New York Academy of Sciences
          Wiley
          0077-8923
          0077-8923
          Dec 2004
          : 1032
          Affiliations
          [1 ] Department of Psychiatry, Mount Sinai School of Medicine, New York, New York, USA. marianne.goodman@med.va.gov
          Article
          1032/1/104
          10.1196/annals.1314.008
          15677398
          eb6d0eeb-dc2c-4275-8c79-c85d91bdba33
          History

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