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Neurosci Biobehav Rev. 2014 Mar;40:6-19. doi: 10.1016/j.neubiorev.2014.01.003. Epub 2014 Jan 20.

Genetics of borderline personality disorder: systematic review and proposal of an integrative model.

Author information

1
Univ Lille Nord de France, CHRU de Lille, F-59000 Lille, France; Laboratoire de Neurosciences Fonctionnelles et Pathologies (LNFP), Université Droit & Santé Lille (UDSL), F-59000 Lille, France; Psychiatry and Pediatric Psychiatry Department, University Medical Centre of Lille (CHULille), F-59037 Lille, France. Electronic address: ali.amad@chru-lille.fr.
2
INSERM U894, Centre de Psychiatrie & Neurosciences, Paris, France.
3
Univ Lille Nord de France, CHRU de Lille, F-59000 Lille, France; Laboratoire de Neurosciences Fonctionnelles et Pathologies (LNFP), Université Droit & Santé Lille (UDSL), F-59000 Lille, France; Psychiatry and Pediatric Psychiatry Department, University Medical Centre of Lille (CHULille), F-59037 Lille, France.
4
INSERM U894, Centre de Psychiatrie & Neurosciences, Paris, France; Sainte-Anne Hospital (Paris-Descartes University), Paris, France.

Abstract

Borderline personality disorder (BPD) is one of the most common mental disorders and is characterized by a pervasive pattern of emotional lability, impulsivity, interpersonal difficulties, identity disturbances, and disturbed cognition. Here, we performed a systematic review of the literature concerning the genetics of BPD, including familial and twin studies, association studies, and gene-environment interaction studies. Moreover, meta-analyses were performed when at least two case-control studies testing the same polymorphism were available. For each gene variant, a pooled odds ratio (OR) was calculated using fixed or random effects models. Familial and twin studies largely support the potential role of a genetic vulnerability at the root of BPD, with an estimated heritability of approximately 40%. Moreover, there is evidence for both gene-environment interactions and correlations. However, association studies for BPD are sparse, making it difficult to draw clear conclusions. According to our meta-analysis, no significant associations were found for the serotonin transporter gene, the tryptophan hydroxylase 1 gene, or the serotonin 1B receptor gene. We hypothesize that such a discrepancy (negative association studies but high heritability of the disorder) could be understandable through a paradigm shift, in which "plasticity" genes (rather than "vulnerability" genes) would be involved. Such a framework postulates a balance between positive and negative events, which interact with plasticity genes in the genesis of BPD.

KEYWORDS:

Borderline personality disorder; Genetics; Gene–environment interaction; Plasticity genes

PMID:
24456942
DOI:
10.1016/j.neubiorev.2014.01.003
[Indexed for MEDLINE]

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