{"title":"产后抑郁症的药物靶点:孟德尔随机化和局部化研究。","authors":"Song Wu, Meihong Shen, Huiyan Wang, Wenbo Zhou","doi":"10.1007/s10571-025-01581-x","DOIUrl":null,"url":null,"abstract":"<p><p>Postpartum depression (PPD) remains a complex disorder with poorly understood genetic underpinnings. This study systematically evaluated the genetic susceptibility of PPD and identified potential therapeutic targets using Mendelian Randomization (MR) approach. Using a two-sample MR approach, the study assessed the causal effects of expression quantitative trait loci (eQTLs) of druggable genes in blood on PPD, which was sourced from the FinnGen. The primary analytical method was the inverse variance weighted, supplemented by a series sensitivity analyses. Summary-data-based Mendelian Randomization (SMR) analysis was used to validate the identified genes, and Bayesian colocalization analysis evaluated shared causal variants and colocalization probabilities between significant targets and PPD. A Phenome-Wide Association Study (PheWAS) was conducted to assess the associations of established PPD markers with other traits to exclude potential side effects. The results showed that the eQTLs of 12 druggable genes were significantly associated with PPD susceptibility. Seven genes were identified as risk factors, and the expression levels of five genes significantly reduced PPD susceptibility. Colocalization analysis supported the hypothesis that PPD may be associated with shared causal variants of ALDH16A1 (OR = 1.09, 95% CI 1.05-1.13, PP.H4 = 0.78) and SLC29A4 (OR = 1.36, 95% CI 1.23-1.50, PP.H4 = 0.76). The PheWAS did not indicate potential side effects for these two therapeutic targets. This study identified new genetic susceptibilities and potential therapeutic targets associated with PPD, providing novel insights for clinical diagnosis and treatment, and offering new research directions for understanding the molecular mechanisms of PPD.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"61"},"PeriodicalIF":4.8000,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179039/pdf/","citationCount":"0","resultStr":"{\"title\":\"Druggable Targets for Postpartum Depression: A Mendelian Randomization and Colocalization Study.\",\"authors\":\"Song Wu, Meihong Shen, Huiyan Wang, Wenbo Zhou\",\"doi\":\"10.1007/s10571-025-01581-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Postpartum depression (PPD) remains a complex disorder with poorly understood genetic underpinnings. This study systematically evaluated the genetic susceptibility of PPD and identified potential therapeutic targets using Mendelian Randomization (MR) approach. Using a two-sample MR approach, the study assessed the causal effects of expression quantitative trait loci (eQTLs) of druggable genes in blood on PPD, which was sourced from the FinnGen. The primary analytical method was the inverse variance weighted, supplemented by a series sensitivity analyses. Summary-data-based Mendelian Randomization (SMR) analysis was used to validate the identified genes, and Bayesian colocalization analysis evaluated shared causal variants and colocalization probabilities between significant targets and PPD. A Phenome-Wide Association Study (PheWAS) was conducted to assess the associations of established PPD markers with other traits to exclude potential side effects. The results showed that the eQTLs of 12 druggable genes were significantly associated with PPD susceptibility. Seven genes were identified as risk factors, and the expression levels of five genes significantly reduced PPD susceptibility. Colocalization analysis supported the hypothesis that PPD may be associated with shared causal variants of ALDH16A1 (OR = 1.09, 95% CI 1.05-1.13, PP.H4 = 0.78) and SLC29A4 (OR = 1.36, 95% CI 1.23-1.50, PP.H4 = 0.76). The PheWAS did not indicate potential side effects for these two therapeutic targets. This study identified new genetic susceptibilities and potential therapeutic targets associated with PPD, providing novel insights for clinical diagnosis and treatment, and offering new research directions for understanding the molecular mechanisms of PPD.</p>\",\"PeriodicalId\":9742,\"journal\":{\"name\":\"Cellular and Molecular Neurobiology\",\"volume\":\"45 1\",\"pages\":\"61\"},\"PeriodicalIF\":4.8000,\"publicationDate\":\"2025-06-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179039/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cellular and Molecular Neurobiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s10571-025-01581-x\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular and Molecular Neurobiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10571-025-01581-x","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
产后抑郁症(PPD)仍然是一种复杂的疾病,人们对其遗传基础知之甚少。本研究系统地评估了PPD的遗传易感性,并使用孟德尔随机化(MR)方法确定了潜在的治疗靶点。该研究采用双样本MR方法,评估了血液中可用药基因的表达数量性状位点(eQTLs)对PPD的因果影响,这些基因来自FinnGen。主要分析方法为方差反加权,辅以一系列敏感性分析。采用基于汇总数据的孟德尔随机化(SMR)分析验证鉴定的基因,贝叶斯共定位分析评估重要靶点与PPD之间的共有因果变异和共定位概率。进行了全现象关联研究(PheWAS),以评估已建立的PPD标志物与其他性状的关联,以排除潜在的副作用。结果显示,12个可用药基因的eqtl与PPD易感性显著相关。7个基因被确定为危险因素,其中5个基因的表达水平显著降低PPD的易感性。共定位分析支持PPD可能与ALDH16A1 (OR = 1.09, 95% CI 1.05-1.13, PP.H4 = 0.78)和SLC29A4 (OR = 1.36, 95% CI 1.23-1.50, PP.H4 = 0.76)的共同因果变异相关的假设。PheWAS没有显示这两个治疗靶点的潜在副作用。本研究发现了与PPD相关的新的遗传易感性和潜在的治疗靶点,为临床诊断和治疗提供了新的见解,并为了解PPD的分子机制提供了新的研究方向。
Druggable Targets for Postpartum Depression: A Mendelian Randomization and Colocalization Study.
Postpartum depression (PPD) remains a complex disorder with poorly understood genetic underpinnings. This study systematically evaluated the genetic susceptibility of PPD and identified potential therapeutic targets using Mendelian Randomization (MR) approach. Using a two-sample MR approach, the study assessed the causal effects of expression quantitative trait loci (eQTLs) of druggable genes in blood on PPD, which was sourced from the FinnGen. The primary analytical method was the inverse variance weighted, supplemented by a series sensitivity analyses. Summary-data-based Mendelian Randomization (SMR) analysis was used to validate the identified genes, and Bayesian colocalization analysis evaluated shared causal variants and colocalization probabilities between significant targets and PPD. A Phenome-Wide Association Study (PheWAS) was conducted to assess the associations of established PPD markers with other traits to exclude potential side effects. The results showed that the eQTLs of 12 druggable genes were significantly associated with PPD susceptibility. Seven genes were identified as risk factors, and the expression levels of five genes significantly reduced PPD susceptibility. Colocalization analysis supported the hypothesis that PPD may be associated with shared causal variants of ALDH16A1 (OR = 1.09, 95% CI 1.05-1.13, PP.H4 = 0.78) and SLC29A4 (OR = 1.36, 95% CI 1.23-1.50, PP.H4 = 0.76). The PheWAS did not indicate potential side effects for these two therapeutic targets. This study identified new genetic susceptibilities and potential therapeutic targets associated with PPD, providing novel insights for clinical diagnosis and treatment, and offering new research directions for understanding the molecular mechanisms of PPD.
期刊介绍:
Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.