Monoamine Oxidase A in Antisocial Personality Disorder and Borderline Personality Disorder.

Monoamine Oxidase A in Antisocial Personality Disorder and Borderline Personality Disorder.
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DOI:
10.1007/s40473-017-0102-0
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发表时间:
2017
影响因子:
1.7
通讯作者:
Vinette SA
Vinette SA
中科院分区:
其他
文献类型:
--
作者:
Kolla NJ;Vinette SA

文献摘要

被引文献

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单胺氧化酶A(MAO-A)基因和MAO-A酶水平的变异与临床和非临床人群中的反社会行为和攻击性有关。在这里,我们提供了一个概述的遗传,表观遗传和神经影像学研究,已审查MAO-A的结构和功能的反社会人格障碍(ASPD)和边缘型人格障碍(BPD)。低活性MAO-A可变核苷酸串联重复序列遗传多态性与大样本的暴力和严重暴力犯罪者(其中许多人患有ASPD)有着密切的联系。最近一项针对ASPD的正电子发射断层扫描(PET)研究同样揭示了被认为与该疾病的精神病理学有关的大脑区域的低MAO-A密度。相比之下,PET还表明BPD患者的脑MAO-A水平升高,并且与情绪低落和自杀倾向的症状有关。候选基因研究已经产生了最令人信服的证据,将MAO-A遗传变异与ASPD和BPD联系起来。尽管如此,文献中仍然存在大量相互矛盾的结果,使得ASPD或BPD与特定的MAO-A遗传变异相关的可能性非常小。未来的研究应该努力研究MAO-A基因型如何与广谱环境影响相互作用,以产生最终可能成为新治疗策略的易处理靶点的脑内表型。
Variation in the monoamine oxidase A (MAO-A) gene and MAO-A enzyme levels have been linked to antisocial behavior and aggression in clinical and non-clinical populations. Here, we provide an overview of the genetic, epigenetic, and neuroimaging research that has examined MAO-A structure and function in antisocial personality disorder (ASPD) and borderline personality disorder (BPD). The low-activity MAO-A variable nucleotide tandem repeat genetic polymorphism has shown a robust association with large samples of violent and seriously violent offenders, many of whom had ASPD. A recent positron emission tomography (PET) study of ASPD similarly revealed low MAO-A density in brain regions thought to contribute to the psychopathology of the condition. By contrast, PET has also demonstrated that brain MAO-A levels are increased in BPD and that they relate to symptoms of low mood and suicidality. Candidate gene studies have produced the most compelling evidence connecting MAO-A genetic variants to both ASPD and BPD. Still, conflicting results abound in the literature, making it highly unlikely that ASPD or BPD is related to a specific MAO-A genetic variant. Future research should strive to examine how MAO-A genotypes interact with broad-spectrum environmental influences to produce brain endophenotypes that may ultimately become tractable targets for novel treatment strategies.