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Panic disorders: The role of genetics and epigenetics

机译：恐慌症：遗传学和表观遗传学的作用

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Panic disorder is characterized by symptoms with abrupt surges of fear with palpitations, sweating, trembling, heat sensations. Considering its disease burden on each individual and on society, understanding its etiology is important. Though no one specific etiology has been known, like other psychiatric disorders, multiple factors such as genetic, environmental, neurobiological, psychopathological factors have been suggested. In this article, we reviewed currently known etiologies and related study results, regarding especially genetic and epigenetic aspects of the panic disorder. Early studies, including twin studies, family studies, adoption studies suggested highly familial trait of panic disorder. Linkage studies, either, found panic disorder is not a single gene disorder but confirmed existence of multiple related genes. Chromosome and candidate gene studies found few related genes, NPY, ADORA2A, COMT, IKBKE . Newer method, genome-wide association studies (GWAS) have been searching for newer genes. No genome-wide significant genes, however, were detected, confirming previously known candidate genes, NPY5R on 4q31.3-32, BDKRB2 on 14q32, instead. Epigenetic modification has also been studied on many different psychiatric disorders. Monoamine oxidase A (MAOA) hypomethylation, taken together with negative life events, showed relation with panic disorder. Glutamate decarbodylases 1 (GAD1) hypomethylation was also specific on panic disorder patients. Relation with noradrenaline transporter (NET) gene SLC6a2 promoter methylation has also been studied. In conclusion, no specific gene or epigenetic pattern can fully explain etiology of panic disorder. Few genes and epigenetic patterns, however, showed strong association with panic disorder compared to healthy controls. Considering its multivariable background, further studies with larger populations can confirm current results and clarify etiologies of panic disorder.
机译：恐慌症的特征是症状突然加重，出现心，出汗，颤抖，热感。考虑到其对每个人和整个社会的疾病负担，了解其病因很重要。尽管还没有人像其他精神病患者那样知道具体的病因，但已经提出了多种因素，例如遗传，环境，神经生物学，精神病理因素。在本文中，我们回顾了当前已知的病因和相关研究结果，特别是关于恐慌症的遗传和表观遗传方面。早期研究包括双生子研究，家庭研究，收养研究表明，恐慌症具有高度的家族特征。连锁研究也发现恐慌症不是单基因疾病，而是证实存在多个相关基因。染色体和候选基因研究发现几乎没有相关基因，NPY，ADORA2A，COMT和IKBKE。更新的方法，全基因组关联研究（GWAS）一直在寻找更新的基因。但是，未检测到全基因组范围内的重要基因，从而确认了先前已知的候选基因，即4q31.3-32上的NPY5R，14q32上的BDKRB2。还对许多不同的精神疾病研究了表观遗传修饰。单胺氧化酶A（MAOA）的甲基化不足，以及负性生活事件，都与恐慌症相关。谷氨酸去甲酸酯酶1（GAD1）的甲基化不足对惊恐症患者也有特异性。还研究了与去甲肾上腺素转运蛋白（NET）基因SLC6a2启动子甲基化的关系。总之，没有特定的基因或表观遗传模式可以完全解释恐慌症的病因。然而，与健康对照相比，很少有基因和表观遗传模式与恐慌症密切相关。考虑到其多变量背景，对更大人群的进一步研究可以证实当前结果并阐明恐慌症的病因。

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