By Mirella S. Miller
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BPD features were assessed on a quantitative scale. Evidence for linkage was found on chromosomes 1, 4, 9 and 18. 0001). To determine the importance of chromosomes 1, 4, 9 and 18 in the development of BPD it is essential that the results are replicated in other samples and that fine-mapping and association studies in these regions are conducted to identify the actual genetic variants. CANDIDATE GENE STUDIES Besides linkage, association is a powerful approach to map genes involved in complex human traits and disorders.
E. et al. (2006) A dopamine transporter polymorphism is a risk factor for borderline personality disorder in depressed patients. , Spellman, M. & Walsh, D. (1993) The Roscommon Family Study. 1. Methods, diagnosis of probands, and risk of schizophrenia in relatives. F. (1967) Borderline personality organization. Journal of the American Psychoanalitical Association, 15, 641-685 Kernberg, O. F. (1975). Borderline conditions and pathological narcissism. New York: Jason Aronson. C. et al. (1995) Family study of early-onset dysthymia - mood and personality-disorders in relatives of outpatients with dysthymia and episodic major depression and normal controls.
If the predisposing environment involves experiences shared by members of the same family (G-C interaction), the estimate of A will be increased (Purcell 2002; Molenaar et al. 1990). G-E interaction can be detected by determining if the heritability of BPD varies in groups with different environmental conditions (for example experiencing sexual abuse). CONCLUSION BPD is a common personality disorder with a prevalence rate of 1 to 2%. The main symptoms are affective instability, identity disturbance, negative relationships and self-harm (impulsivity).