{"title":"MeCP2和PTEN基因在特异性学习障碍分子基础中的表达改变。","authors":"Fatma Atasever, Nil Özbilüm Şahin, Cansu Mercan Işık","doi":"10.1007/s12031-025-02370-3","DOIUrl":null,"url":null,"abstract":"<p><p>Specific learning disorders (SLD) are neurodevelopmental disorders that affect cognitive abilities such as reading, writing, and mathematics. The molecular mechanisms underlying SLD remain unclear, though genetic and epigenetic factors are thought to play a significant role. MeCP2 is an epigenetic regulator that binds to methylated DNA, playing a crucial role in the regulation of gene expression and SP in neuronal cells. PTEN, a tumor suppressor gene, regulates cell growth, survival, and apoptosis, and is critical for maintaining synaptic integrity. In this study, we aimed to examine the expression of MeCP2 and PTEN in individuals with SLD. RNA was isolated from blood samples, and gene expression was assessed using quantitative PCR (qPCR). A total of 38 participants with SLD and 35 healthy controls were included in the study. Our results revealed a 15.44-fold upregulation of MeCP2 and a 13.66-fold downregulation of PTEN in the SLD group compared to controls, suggesting a disrupted balance of gene expression. There was no significant difference in gene expression between severe and non-severe SLD groups. These findings suggest that the dysregulation of MeCP2 and PTEN may be involved in the pathophysiology of SLD, influencing SP and neuronal function. In conclusion, the altered expression of these genes in individuals with SLD highlights potential biomarkers for early diagnosis and therapeutic targets, opening avenues for future research and intervention strategies.</p>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"74"},"PeriodicalIF":2.8000,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144048/pdf/","citationCount":"0","resultStr":"{\"title\":\"Altered Expression of MeCP2 and PTEN Genes in the Molecular Basis of Specific Learning Disorder.\",\"authors\":\"Fatma Atasever, Nil Özbilüm Şahin, Cansu Mercan Işık\",\"doi\":\"10.1007/s12031-025-02370-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Specific learning disorders (SLD) are neurodevelopmental disorders that affect cognitive abilities such as reading, writing, and mathematics. The molecular mechanisms underlying SLD remain unclear, though genetic and epigenetic factors are thought to play a significant role. MeCP2 is an epigenetic regulator that binds to methylated DNA, playing a crucial role in the regulation of gene expression and SP in neuronal cells. PTEN, a tumor suppressor gene, regulates cell growth, survival, and apoptosis, and is critical for maintaining synaptic integrity. In this study, we aimed to examine the expression of MeCP2 and PTEN in individuals with SLD. RNA was isolated from blood samples, and gene expression was assessed using quantitative PCR (qPCR). A total of 38 participants with SLD and 35 healthy controls were included in the study. Our results revealed a 15.44-fold upregulation of MeCP2 and a 13.66-fold downregulation of PTEN in the SLD group compared to controls, suggesting a disrupted balance of gene expression. There was no significant difference in gene expression between severe and non-severe SLD groups. These findings suggest that the dysregulation of MeCP2 and PTEN may be involved in the pathophysiology of SLD, influencing SP and neuronal function. In conclusion, the altered expression of these genes in individuals with SLD highlights potential biomarkers for early diagnosis and therapeutic targets, opening avenues for future research and intervention strategies.</p>\",\"PeriodicalId\":652,\"journal\":{\"name\":\"Journal of Molecular Neuroscience\",\"volume\":\"75 2\",\"pages\":\"74\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-06-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144048/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Molecular Neuroscience\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12031-025-02370-3\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Molecular Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12031-025-02370-3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Altered Expression of MeCP2 and PTEN Genes in the Molecular Basis of Specific Learning Disorder.
Specific learning disorders (SLD) are neurodevelopmental disorders that affect cognitive abilities such as reading, writing, and mathematics. The molecular mechanisms underlying SLD remain unclear, though genetic and epigenetic factors are thought to play a significant role. MeCP2 is an epigenetic regulator that binds to methylated DNA, playing a crucial role in the regulation of gene expression and SP in neuronal cells. PTEN, a tumor suppressor gene, regulates cell growth, survival, and apoptosis, and is critical for maintaining synaptic integrity. In this study, we aimed to examine the expression of MeCP2 and PTEN in individuals with SLD. RNA was isolated from blood samples, and gene expression was assessed using quantitative PCR (qPCR). A total of 38 participants with SLD and 35 healthy controls were included in the study. Our results revealed a 15.44-fold upregulation of MeCP2 and a 13.66-fold downregulation of PTEN in the SLD group compared to controls, suggesting a disrupted balance of gene expression. There was no significant difference in gene expression between severe and non-severe SLD groups. These findings suggest that the dysregulation of MeCP2 and PTEN may be involved in the pathophysiology of SLD, influencing SP and neuronal function. In conclusion, the altered expression of these genes in individuals with SLD highlights potential biomarkers for early diagnosis and therapeutic targets, opening avenues for future research and intervention strategies.
期刊介绍:
The Journal of Molecular Neuroscience is committed to the rapid publication of original findings that increase our understanding of the molecular structure, function, and development of the nervous system. The criteria for acceptance of manuscripts will be scientific excellence, originality, and relevance to the field of molecular neuroscience. Manuscripts with clinical relevance are especially encouraged since the journal seeks to provide a means for accelerating the progression of basic research findings toward clinical utilization. All experiments described in the Journal of Molecular Neuroscience that involve the use of animal or human subjects must have been approved by the appropriate institutional review committee and conform to accepted ethical standards.