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拷贝数变异在青少年肌阵挛性癫痫中的意外作用。

The unexpected role of copy number variations in juvenile myoclonic epilepsy.

机构信息

Department of Neuropediatrics, University Medical Center Schleswig-Holstein, Christian-Albrechts University, Kiel, Germany.

出版信息

Epilepsy Behav. 2013 Jul;28 Suppl 1:S66-8. doi: 10.1016/j.yebeh.2012.07.005.

Abstract

Structural genomic variants or copy number variants (CNVs) comprise submicroscopic deletions and duplications of chromosomal material, including both rearrangements at genomic hotspots as well as duplications and deletions with unique breakpoints. Copy number variants have increasingly been recognized in the Idiopathic/Genetic Generalized Epilepsies (IGE/GGE) including juvenile myoclonic epilepsy (JME). Microdeletions at 15q13.3, 15q11.2, and 16p13.11 are genetic risk factors that can be identified in 3% of patients with IGE including JME. These microdeletions, however, also represent genetic risk factors to a broad range of other neurodevelopmental disorders. Additionally, 6% of patients with GGE carry other, potentially pathogenic structural genomic variants. While family studies largely support the channelopathy concept of the idiopathic epilepsies, the results of studies investigating copy number variations suggest that JME genetically overlaps with a broad range of other neurodevelopmental disorders. In addition, the particular genetic properties of structural genomic variations as rare genetic variants highlight the complexity of the genetic architecture of human disease.

摘要

结构基因组变异或拷贝数变异 (CNVs) 包括染色体物质的亚微观缺失和重复,包括基因组热点的重排以及具有独特断点的重复和缺失。拷贝数变异在特发性/遗传性全面性癫痫(IGE/GGE)中,包括青少年肌阵挛性癫痫(JME)中越来越受到关注。15q13.3、15q11.2 和 16p13.11 的微缺失是遗传风险因素,可在 3%的 IGE 患者中包括 JME 中识别出来。然而,这些微缺失也代表了广泛的其他神经发育障碍的遗传风险因素。此外,6%的 GGE 患者携带其他潜在致病性结构基因组变异。虽然家族研究在很大程度上支持了特发性癫痫的通道病概念,但研究拷贝数变异的结果表明,JME 在遗传上与广泛的其他神经发育障碍重叠。此外,结构基因组变异作为罕见遗传变异的特殊遗传特性突出了人类疾病遗传结构的复杂性。

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