Aug 2026· Seizure· Vol 141, pp.
276-284
· 0 citations· 36 references
Medicine
TL;DR
This is the second report of autosomal recessive epilepsy associated with biallelic CACNB4 variants and genetic investigations play a crucial role in identifying mutation hotspots, facilitating more accurate diagnoses and enhancing the design of diagnostic panels for early detection.
Abstract
Objective
Epilepsy is a heterogeneous group of neurological disorders characterized by recurrent seizures with diverse clinical manifestations. Seizures are classified based on their onset and semiology as focal, generalized, or unknown onset, whereas epilepsy syndromes are defined by specific electroclinical features, age at onset, and etiological factors. In this study, we investigated the diagnostic utility of whole-exome sequencing (WES) in two consanguineous families presenting with epilepsy and neurological manifestations segregating in an autosomal recessive manner.
Methods
Two affected members of family 1 and one affected member from family 2 underwent whole-exome sequencing (WES). The sequencing data were analyzed using an in-house bioinformatics pipeline to identify potential disease-causing variants. Bidirectional Sanger sequencing was performed to examine the co-segregation of the investigated variants. To further evaluate the pathogenicity of the identified variants, 3D protein modeling and several in silico tools were used.
Results
We studied two consanguineous families with multiple affected individuals manifesting epilepsy, consistent with autosomal recessive inheritance. WES of family 1 identified a novel homozygous, presumably deleterious, missense variant c.839T>C:p.(Ile280Thr), in CACNB4 (NM_000726.3). Family 2 also harbored a novel homozygous, presumably deleterious, missense variant, c.1199G>A;p.(Arg400His). Both variants affect highly conserved residues. 3D modeling suggested that the mutant proteins required longer time to stabilize and exhibited increased structural flexibility. Both variants resulted in less compact protein structures with an expanded central cavity (∼10 Å larger), thereby altering the overall conformation.
Significance
To our knowledge, this is the second report of autosomal recessive epilepsy associated with biallelic CACNB4 variants. Epilepsy is often a multigenic disorder, which makes clinical diagnosis challenging. Genetic investigations play a crucial role in identifying mutation hotspots, facilitating more accurate diagnoses and enhancing the design of diagnostic panels for early detection.
This study may expand the mutation and phenotypic spectrum of SETD1A-related disorders, establishing the relationship between SETD1A variants and isolated early-onset epilepsy without accompanying severe neurodevelopmental deficits, and highlighting the value of genetic testing in infants with unexplained epilepsy.
Rina Su, Lei Zhu, Lin Jiang et al.· Frontiers in Neuroscience· 0 citations
Aim: Identify new genetic variants linked to neurodevelopmental disorders to be used in routine genetic diagnostics. Methods: Whole exome sequencing (WES) was used for ten unrelated families from Jordan characterized by one or two affected members with neurodevelopmental disorders (NDDs), in which the parents are consanguineous in nine families. Results: Ten variants are identified in this study; one variant per family. Eight variants are identified by cross-link with the pathogenic variants in ClinVar and in our in-house database, and two variants are identified for the first time. Nine of the total identified variants are homozygous in the nine consanguineous families and one variant is heterozygous in the non-consanguineous family. Three of the identified variants were previously reported in unrelated Jordanian families compared to the families in this study. These three variants are NM_018359.5:c.344T>A;p.Val115Glu in the gene UFSP2, NM_000487.6:c.256C>G;p.Arg86Gly in the gene ARSA and NM_017882.3:c.144G>A;p.Trp48* in the gene CLN6. The variants that are identified for the first time are splicing variants; splice donor variant NM_000433.4:c.366+1G>C in the gene NCF2 and splice acceptor variant NM_000191.3:c.498-1G>A in the gene HMGCL. Conclusions: The results of this study stress the importance of continuous research using WES for NDDs in Jordan to identify new variants.
T. Froukh, Eman Albsoul· Exploration of Neuroprotecti...· 0 citations
This study has diagnosed a case of developmental and epileptic encephalopathy 32 by WGS and enriched the mutational spectrum of the KCNA2 gene and provided guidance for preimplantation genetic testing and counseling for the pedigree.
Lulu Gao, Peiwen Xu, Jie Li et al.· Zhonghua yi xue yi chuan xue...· 0 citations
This study shows that individual oligogenic analysis is implementable in selected patients and represents a feasible addition to monogenic analysis, and could not identify any definite oligogenic combination.
Sarah Duerinckx, Barbara Gravel, J. Soblet et al.· Epilepsia· 0 citations
The study expands the phenotypic heterogeneity of A–T and extends the allelic spectrum of ATM variants by recruiting a consanguineous Pakistani family with multiple individuals having adolescent‐onset ataxia.
Faiza Aslam, Weizhen Ji, L. Jeffries et al.· Genetics Research· 0 citations