{"title":"Transcriptional signatures of cortical structural changes in chronic insomnia disorder.","authors":"Liyong Yu, Daijie Hu, Yucai Luo, Wenting Lin, Hao Xu, Xiangwen Xiao, Zihao Xia, Zeyang Dou, Guangli Zhao, Lu Yang, Dezhong Peng, Qi Zhang, Siyi Yu","doi":"10.1111/psyp.14671","DOIUrl":null,"url":null,"abstract":"<p><p>Chronic insomnia disorder (CID) is a multidimensional disease that may influence various levels of brain organization, spanning the macroscopic structural connectome to microscopic gene expression. However, the connection between genomic variations and morphological alterations in CID remains unclear. Here, we investigated brain structural changes in CID patients at the whole-brain level and whether these link to transcriptional characteristics. Brain structural data from 104 CID patients and 102 matched healthy controls (HC) were acquired to examine cortical structural alterations using morphometric similarity (MS) analysis. Partial least squares (PLS) regression and transcriptome data from the Allen Human Brain Atlas were used to extract genomes related to MS changes. Gene-category enrichment analysis (GCEA) was used to identify potential molecular mechanisms behind the observed structural changes. We found that CID patients exhibited MS reductions in the parietal and limbic regions, along with enhancements in the temporal and frontal regions compared to HCs (p<sub>FDR</sub> < .05). Subsequently, PLS and GCEA revealed that these MS alterations were spatially correlated with a set of genes, especially those significantly correlated with excitatory and inhibitory neurons and chronic neuroinflammation. This neuroimaging-transcriptomic study bridges the gap between cortical structural changes and the molecular mechanisms in CID patients, providing novel insight into the pathophysiology of insomnia and targeted treatments.</p>","PeriodicalId":20913,"journal":{"name":"Psychophysiology","volume":" ","pages":"e14671"},"PeriodicalIF":2.9000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Psychophysiology","FirstCategoryId":"102","ListUrlMain":"https://doi.org/10.1111/psyp.14671","RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/19 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Chronic insomnia disorder (CID) is a multidimensional disease that may influence various levels of brain organization, spanning the macroscopic structural connectome to microscopic gene expression. However, the connection between genomic variations and morphological alterations in CID remains unclear. Here, we investigated brain structural changes in CID patients at the whole-brain level and whether these link to transcriptional characteristics. Brain structural data from 104 CID patients and 102 matched healthy controls (HC) were acquired to examine cortical structural alterations using morphometric similarity (MS) analysis. Partial least squares (PLS) regression and transcriptome data from the Allen Human Brain Atlas were used to extract genomes related to MS changes. Gene-category enrichment analysis (GCEA) was used to identify potential molecular mechanisms behind the observed structural changes. We found that CID patients exhibited MS reductions in the parietal and limbic regions, along with enhancements in the temporal and frontal regions compared to HCs (pFDR < .05). Subsequently, PLS and GCEA revealed that these MS alterations were spatially correlated with a set of genes, especially those significantly correlated with excitatory and inhibitory neurons and chronic neuroinflammation. This neuroimaging-transcriptomic study bridges the gap between cortical structural changes and the molecular mechanisms in CID patients, providing novel insight into the pathophysiology of insomnia and targeted treatments.
慢性失眠症(CID)是一种多维疾病,可能影响大脑组织的各个层面,从宏观的结构连接组到微观的基因表达。然而,CID 基因组变异与形态学改变之间的联系仍不清楚。在此,我们从全脑水平研究了CID患者的脑结构变化以及这些变化是否与转录特征有关。我们获取了104名CID患者和102名匹配的健康对照组(HC)的脑结构数据,利用形态计量相似性(MS)分析来研究皮质结构的改变。利用偏最小二乘法(PLS)回归和艾伦人脑图谱(Allen Human Brain Atlas)的转录组数据提取与MS变化相关的基因组。基因类别富集分析(GCEA)用于确定观察到的结构变化背后的潜在分子机制。我们发现,与 HCs 相比,CID 患者顶叶区和边缘区的 MS 减少,而颞叶区和额叶区的 MS 增加(pFDR
期刊介绍:
Founded in 1964, Psychophysiology is the most established journal in the world specifically dedicated to the dissemination of psychophysiological science. The journal continues to play a key role in advancing human neuroscience in its many forms and methodologies (including central and peripheral measures), covering research on the interrelationships between the physiological and psychological aspects of brain and behavior. Typically, studies published in Psychophysiology include psychological independent variables and noninvasive physiological dependent variables (hemodynamic, optical, and electromagnetic brain imaging and/or peripheral measures such as respiratory sinus arrhythmia, electromyography, pupillography, and many others). The majority of studies published in the journal involve human participants, but work using animal models of such phenomena is occasionally published. Psychophysiology welcomes submissions on new theoretical, empirical, and methodological advances in: cognitive, affective, clinical and social neuroscience, psychopathology and psychiatry, health science and behavioral medicine, and biomedical engineering. The journal publishes theoretical papers, evaluative reviews of literature, empirical papers, and methodological papers, with submissions welcome from scientists in any fields mentioned above.