Autosomal dominant lateral temporal epilepsy (ADLTE) is an inherited syndrome caused by mutations in the leucine-rich glioma inactivated 1 (LGI1) gene. In a family with six ADLTE patients spanning four generations, our linkage and exome sequencing investigations revealed a rare frameshift heterozygous mutation in LGI1 (c.1494del(p.Phe498LeufsTer15)). Gene cloning methods were used to create plasmids with wild-type and mutant LGI1 alleles. Through transfection of HEK293 cells and primary neurons, they were utilized to assess the subcellular location of wild-type and mutant LGI1. Moreover, the plasmid-transfected primary neurons were analyzed for neuronal complexity and density of dendritic spines. According to our results. the mutation decreased LGI1 secretion in transfected HEK293 cells. In primary neurons, mutant LGI1 affected neuronal polarity and complexity. Our findings have broadened the phenotypic spectrum of LGI1 mutations and provided evidence regarding the pathogenicity of this mutation. In addition, we discovered new information about the role of LGI1 in the development of temporal lobe epilepsy, along with a possible link between neuronal polarity disorder and ADLTE.
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http://dx.doi.org/10.1016/j.neulet.2022.136698 | DOI Listing |
Heliyon
July 2023
Department of Pharmacology, Faculty of Pharmacy, Osaka Medical and Pharmaceutical University, Takatsuki, Osaka, 569-1094, Japan.
() was identified as a causative gene of autosomal dominant lateral temporal lobe epilepsy. We previously reported that -mutant rats carrying a missense mutation (L385R) showed audiogenic seizure-susceptibility. To explore the pathophysiological mechanisms underlying Lgi1-related epilepsy, we evaluated changes in glutamate and GABA release in -mutant rats.
View Article and Find Full Text PDFCell Biosci
February 2023
School of Life Sciences, Henan University, Kaifeng, 475004, China.
Background: Autosomal dominant lateral temporal epilepsy (ADLTE) is an inherited syndrome caused by mutations in the leucine-rich glioma inactivated 1 (LGI1) gene. It is known that functional LGI1 is secreted by excitatory neurons, GABAergic interneurons, and astrocytes, and regulates AMPA-type glutamate receptor-mediated synaptic transmission by binding ADAM22 and ADAM23. However, > 40 LGI1 mutations have been reported in familial ADLTE patients, more than half of which are secretion-defective.
View Article and Find Full Text PDFNeurosci Lett
June 2022
Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, Chongqing 400016, China. Electronic address:
Autosomal dominant lateral temporal epilepsy (ADLTE) is an inherited syndrome caused by mutations in the leucine-rich glioma inactivated 1 (LGI1) gene. In a family with six ADLTE patients spanning four generations, our linkage and exome sequencing investigations revealed a rare frameshift heterozygous mutation in LGI1 (c.1494del(p.
View Article and Find Full Text PDFFASEB J
March 2022
Minister of Education Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Medical School, Nanjing University, Nanjing, China.
Leucine-rich glioma-inactivated protein 1 (LGI1) is known to play a key role in autosomal dominant lateral temporal lobe epilepsy (ADLTE). The ADLTE is an inherited disease characterized by focal seizures with distinctive auditory or aphasic symptoms. A large number of mutations on the Lgi1 gene have been reported and are believed to be the genetic cause for ADLTE.
View Article and Find Full Text PDFCNS Neurosci Ther
February 2022
Department of Prenatal Diagnosis, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health care Hospital, Nanjing, China.
Aims: This study aimed to explore the pathomechanism of a mutation on the leucine-rich glioma inactivated 1 gene (LGI1) identified in a family having autosomal dominant lateral temporal lobe epilepsy (ADLTE), using a precise knock-in mouse model.
Methods And Results: A novel LGI1 mutation, c.152A>G; p.
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