癫痫
桑格测序
胡说
错义突变
医学
病因学
遗传学
基因检测
异源双工
遗传咨询
遗传诊断
儿科
癫痫综合征
复合杂合度
基因分型
基因
声音恐惧症
神经系统疾病
生物信息学
家族史
候选基因
临床诊断
无义突变
索引案例
遗传分析
基因型
等位基因
遗传倾向
作者
Ayman Kilany,Eman E.A. Mohammed,Tamer H. A. Ammar,Nahla N. Elmalah,Mohamed Agha,Abd Elwaged Mohamed Asmaa,Shora Mostafa
标识
DOI:10.21608/ejchem.2025.407056.12103
摘要
Background Epilepsy is a prevalent and heterogeneous neurological disorder, defined by an enduring predisposition to generate unprovoked epileptic seizures, accompanied by significant neurobiological, cognitive, psychological, and social consequences. It represents the most frequent chronic neurological condition in childhood, affecting approximately 0.5%−1% of children globally. Given its diverse etiologies, molecular diagnosis is crucial for effective management and prognostication.ObjectivesThis study aimed to investigate the clinical characteristics and define the underlying genetic etiology of hereditary epilepsy in three unrelated Egyptian families using Whole-Exome Sequencing (WES) as a primary diagnostic tool.Subjects and Methods Five patients with epilepsy from three unrelated Egyptian families were enrolled. WES was initially performed on one index patient from each family. Subsequent segregation analysis, utilizing PCR amplification followed by Sanger sequencing, was extended to affected relatives whenever possible. ResultsWES successfully identified three distinct variants across three different genes. A novel likely pathogenic homozygous nonsense variant, c.912G>A; p.(Trp304*) (NM_000218.3) in the KCNQ1 gene was identified in patients 1 and 2 (Family 1). This novel variant was confirmed to be absent from HGMD, ClinVar, and gnomAD databases. Two previously reported variants were also detected: the pathogenic heterozygous missense c.1181C>T; p.(Ala394Val) (NM_001165963.4) in the SCN1A gene in patients 3 and 4 (Family 2), and the likely pathogenic heterozygous missense c.335C>T; p.(Thr112Ile) (NM_003002.4) in the SDHD gene in patient 5 (Family 3). We note that segregation analysis could not be performed for F1and F3 due to the unavailability of parental DNA, which limits the diagnosis confidence in these familiesConclusionWES proved to be an efficient diagnostic strategy for elucidating the complex, heterogeneous molecular etiology of hereditary epilepsy, particularly in cases lacking a prior genetic diagnosis. Our findings successfully established a molecular diagnosis for the included patients, identified a novel pathogenic variant, and underscored the considerable molecular diversity underlying epilepsy and associated neurological phenotypes within this specific Egyptian cohort.
科研通智能强力驱动
Strongly Powered by AbleSci AI