División Académica Multidisciplinaria de Jalpa de Méndez, Universidad Juárez Autónoma de Tabasco, Jalpa de Méndez 86205, Mexico.
Hospital Psiquiátrico Infantil "Juan N. Navarro", Tlalpan 14080, Mexico.
Genes (Basel). 2024 Aug 4;15(8):1025. doi: 10.3390/genes15081025.
BACKGROUND: Alexithymia is a trait involving difficulties in processing emotions. Genetic association studies have investigated candidate genes involved in alexithymia's pathogenesis. Therefore, the aim of the present study was to perform a systematic review of the genetic background associated with alexithymia. METHODS: A systematic review of genetic studies of people with alexithymia was conducted. Electronic databases including PubMed, Scopus, and Web of Science were searched for the study purpose. We used the words "Alexithymia", "gene", "genetics", "variants", and "biomarkers". The present systematic review was performed following the Preferred Reporting Items for Systematic reviews and Meta-Analyses statement. We found only candidate gene studies. A total of seventeen studies met the eligibility criteria, which comprised 22,361 individuals. The candidate genes associated with alexithymia were the serotoninergic pathway genes solute carrier family 6 member 4 (), serotonin 1A receptor (), and serotonin 1A receptor (); the neurotransmitter metabolism genes dopamine receptor D2 (), ankyrin repeat and kinase domain containing 1 (), catechol-o-methyltransferase (), brain-derived neurotrophic factor (), and oxytocin receptor (); and other pathway genes, vitamin D-binding protein (), tumor protein P53 regulated apoptosis inducing protein 1 (), Rho GTPase Activating Protein 32 (), and transmembrane protein 88B (). CONCLUSION: The results of this study showed that only case-control gene studies have been performed in alexithymia. On the basis of our findings, the majority of alexithymia genes and polymorphisms in this study belong to the serotoninergic pathway and neurotransmitter metabolism genes. These data suggest a role of serotoninergic neurotransmission in alexithymia. Nevertheless, more and future research is required to learn about the role of these genes in alexithymia.
背景:述情障碍是一种涉及情绪处理困难的特质。遗传关联研究已经调查了参与述情障碍发病机制的候选基因。因此,本研究的目的是对与述情障碍相关的遗传背景进行系统综述。
方法:对述情障碍患者的遗传研究进行了系统综述。电子数据库包括 PubMed、Scopus 和 Web of Science 被用于研究目的。我们使用了“述情障碍”、“基因”、“遗传学”、“变体”和“生物标志物”等词。本系统综述遵循系统评价和荟萃分析报告的首选项目进行。我们只发现了候选基因研究。共有 17 项研究符合纳入标准,共纳入 22361 人。与述情障碍相关的候选基因包括 5-羟色胺能途径基因溶质载体家族 6 成员 4()、5-羟色胺 1A 受体()和 5-羟色胺 1A 受体();神经递质代谢基因多巴胺受体 D2()、锚蛋白重复和激酶结构域包含蛋白 1()、儿茶酚-O-甲基转移酶()、脑源性神经营养因子()和催产素受体();以及其他途径基因,维生素 D 结合蛋白()、肿瘤蛋白 P53 调节凋亡诱导蛋白 1()、Rho GTP 酶激活蛋白 32()和跨膜蛋白 88B()。
结论:本研究结果表明,只有病例对照基因研究在述情障碍中进行。基于我们的发现,本研究中大多数述情障碍基因和多态性属于 5-羟色胺能途径和神经递质代谢基因。这些数据表明 5-羟色胺能神经传递在述情障碍中起作用。然而,需要更多和未来的研究来了解这些基因在述情障碍中的作用。
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