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

被引:111
作者
Amad, Ali [1 ,2 ,3 ]
Ramoz, Nicolas [4 ]
Thomas, Pierre [1 ,2 ,3 ]
Jardri, Renaud [1 ,2 ,3 ]
Gorwood, Philip [4 ,5 ]
机构
[1] Univ Lille Nord France, CHRU Lille, F-59000 Lille, France
[2] UDSL, LNFP, F-59000 Lille, France
[3] Univ Med Ctr Lille CHULille, Psychiat & Pediat Psychiat Dept, F-59037 Lille, France
[4] INSERM, U894, Ctr Psychiat & Neurosci, Paris, France
[5] Paris Descartes Univ, St Anne Hosp, Paris, France
关键词
Borderline personality disorder; Genetics; Gene-environment interaction; Plasticity genes; SEROTONIN TRANSPORTER GENE; ENVIRONMENTAL RISK-FACTORS; O-METHYLTRANSFERASE COMT; CHILDHOOD SEXUAL-ABUSE; SERIOUS LIFE EVENTS; DIMENSIONAL REPRESENTATIONS; IMPULSIVE AGGRESSION; RECEPTOR GENE; AXIS-I; GLUCOCORTICOID-RECEPTOR;
D O I
10.1016/j.neubiorev.2014.01.003
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:6 / 19
页数:14
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