Background

The identification of bipolar disorder (BD) type II patients has both treatment and prognostic implications. Better understanding of its underlying genetics may yield useful diagnostic tools.

Methods

A systematic review on BDII genetics was done using articles published in 2009–2019, following PRISMA recommendations.

Results

The most studied polymorphism was BDNF Val66Met with several gene-gene interactions within the dopaminergic system. Associations were reported within the monoaminergic systems (DRD3, ADH1B and SLC6A4), calcium (CACNB2 and CACNG2) and cAMP (PDE1DA, PDE4B and DISC1) signal transduction pathways and the immune system (TNFα, IFNδ and IL-10). Chromosomes 2, 3 and 10 were associated with BDII and polygenic risk scores distinguished between BD subtypes and with major depressive disorder.

Conclusions

Research on BDII stems from BDI findings, however with a stronger contribution of gene-gene interactions and low-effect alleles on known neuroplasticity and monoaminergic system genes. Genome studies point to transdiagnostic backgrounds, with wider associations across bipolar spectrum disorders. Findings able to accurately differentiate BDII remain elusive, dependent on better phenotypic characterization and new research methods.

中文翻译：

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躁郁症亚型之间的遗传差异：一项针对II型躁郁症的系统评价。

背景

II型双相情感障碍（BD）患者的鉴定对治疗和预后都有影响。更好地了解其潜在遗传学可能会产生有用的诊断工具。

方法

根据PRISMA的建议，使用2009-2019年发表的文章对BDII遗传学进行了系统的综述。

结果

最多人研究的多态性是BDNF Val66Met，在多巴胺能系统内具有几种基因-基因相互作用。据报道在单胺能系统（DRD3 ，ADH1B和SLC6A4），钙（CACNB2和CACNG2）和cAMP（PDE1DA，PDE4B和DISC1）信号转导途径与免疫系统（TNFα，IFNδ和IL-10）之间存在关联。染色体2、3和10与BDII和BD亚型之间以及多发性抑郁症之间的多基因风险评分有所不同。

结论

BDII的研究源于BDI的发现，然而，基因-基因相互作用和低等位基因对已知的神经可塑性和单胺能系统基因的贡献更大。基因组研究指向跨诊断背景，跨双相性谱系障碍的关联更广泛。取决于更好的表型表征和新的研究方法，能够准确区分BDII的发现仍然难以捉摸。