Suppr超能文献

MeCP2和PTEN基因表达改变在特定学习障碍分子基础中的作用

Altered Expression of MeCP2 and PTEN Genes in the Molecular Basis of Specific Learning Disorder.

作者信息

Atasever Fatma, Şahin Nil Özbilüm, Işık Cansu Mercan

机构信息

Department of Molecular Biology and Genetic, Faculty of Science, Sivas Cumhuriyet University, 58140, Sivas, Turkey.

Department of Child and Adolescent Psychiatry, Faculty of Medicine, Sivas Cumhuriyet University, Sivas, Turkey.

出版信息

J Mol Neurosci. 2025 Jun 6;75(2):74. doi: 10.1007/s12031-025-02370-3.

Abstract

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.

摘要

特定学习障碍(SLD)是一种神经发育障碍,会影响阅读、写作和数学等认知能力。尽管遗传和表观遗传因素被认为起着重要作用,但SLD背后的分子机制仍不清楚。MeCP2是一种表观遗传调节因子,可与甲基化DNA结合,在神经元细胞的基因表达和突触可塑性(SP)调节中起关键作用。PTEN是一种肿瘤抑制基因,可调节细胞生长、存活和凋亡,对维持突触完整性至关重要。在本研究中,我们旨在检测SLD个体中MeCP2和PTEN的表达。从血液样本中分离RNA,并使用定量PCR(qPCR)评估基因表达。共有38名SLD参与者和35名健康对照者纳入本研究。我们的结果显示,与对照组相比,SLD组中MeCP2上调了15.44倍,PTEN下调了13.66倍,表明基因表达平衡被破坏。重度和非重度SLD组之间的基因表达没有显著差异。这些发现表明,MeCP2和PTEN失调可能参与了SLD的病理生理过程,影响突触可塑性和神经元功能。总之,SLD个体中这些基因表达的改变突出了早期诊断的潜在生物标志物和治疗靶点,为未来的研究和干预策略开辟了道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9592/12144048/2a424ef708d3/12031_2025_2370_Fig1_HTML.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验