Association of sodium voltage-gated channel genes polymorphisms with epilepsy risk and prognosis in the Saudi population.


Journal

Annals of medicine
ISSN: 1365-2060
Titre abrégé: Ann Med
Pays: England
ID NLM: 8906388

Informations de publication

Date de publication:
12 2022
Historique:
entrez: 8 7 2022
pubmed: 9 7 2022
medline: 12 7 2022
Statut: ppublish

Résumé

Epilepsy is a heterogeneous complex condition that involve the human brain. Genetic predisposition to epilepsy is a fundamental factor of the disorder aetiology. The sodium voltage-gated channel (SCN) genes variants are critical biomarker for the epilepsy development and progression. In this study, we aimed to investigate the association of several SNCs genetic polymorphisms with epilepsy risk and their intrudance of the disease prognosis. Blood samples were withdrawn from 296 Epilepsy patients in addition to 293 healthy matched participants prior to DNA extraction. PCR-sequencing was used for genotyping analysis. Genotyping outputs were then statistically analysed for genotype/phenotype evaluation. Within SCN1A gene we found that the rs6432861 ( In light of our results, we infer that SCN genes polymorphisms are strong candidates for epilepsy development and progression. Furthermore, these variant are essential for the disorder prognosis and medications outcomes.Key MessagesGenetic polymorphisms of sodium channels SCN1A, SCN2A and SCN3A were found to be associated with the risk of epilepsy.SCN1B polymorphisms were found to be correlated to epilepsy reduced risk.SCNs variants are involved in the epilepsy prognosis and response to treatment.

Sections du résumé

BACKGROUND
Epilepsy is a heterogeneous complex condition that involve the human brain. Genetic predisposition to epilepsy is a fundamental factor of the disorder aetiology. The sodium voltage-gated channel (SCN) genes variants are critical biomarker for the epilepsy development and progression. In this study, we aimed to investigate the association of several SNCs genetic polymorphisms with epilepsy risk and their intrudance of the disease prognosis.
METHODS
Blood samples were withdrawn from 296 Epilepsy patients in addition to 293 healthy matched participants prior to DNA extraction. PCR-sequencing was used for genotyping analysis. Genotyping outputs were then statistically analysed for genotype/phenotype evaluation.
RESULTS
Within SCN1A gene we found that the rs6432861 (
CONCLUSION
In light of our results, we infer that SCN genes polymorphisms are strong candidates for epilepsy development and progression. Furthermore, these variant are essential for the disorder prognosis and medications outcomes.Key MessagesGenetic polymorphisms of sodium channels SCN1A, SCN2A and SCN3A were found to be associated with the risk of epilepsy.SCN1B polymorphisms were found to be correlated to epilepsy reduced risk.SCNs variants are involved in the epilepsy prognosis and response to treatment.

Identifiants

pubmed: 35801810
doi: 10.1080/07853890.2022.2096257
pmc: PMC9367647
doi:

Substances chimiques

NAV1.1 Voltage-Gated Sodium Channel 0
NAV1.2 Voltage-Gated Sodium Channel 0
NAV1.3 Voltage-Gated Sodium Channel 0
SCN1A protein, human 0
SCN1B protein, human 0
SCN2A protein, human 0
SCN3A protein, human 0
Sodium Channels 0
Voltage-Gated Sodium Channel beta-1 Subunit 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1938-1951

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Auteurs

Mansour A Alghamdi (MA)

Department of Anatomy, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Genomics and Personalized Medicine Unit, College of Medicine, King Khalid University, Abha, Saudi Arabia.

Laith N Al-Eitan (LN)

Department of Applied Biological Sciences, Jordan University of Science and Technology, Irbid, Jordan.
Department of Biotechnology and Genetic Engineering, Jordan University of Science and Technology, Irbid, Jordan.

Ashwag Asiri (A)

Department of Child Health, College of Medicine, King Khalid University, Abha, Saudi Arabia.

Doaa M Rababa'h (DM)

Department of Applied Biological Sciences, Jordan University of Science and Technology, Irbid, Jordan.

Sultan A Alqahtani (SA)

Neurology Department, Neuroscience Centre, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.

Mohammed S Aldarami (MS)

Neurology Department, Neuroscience Centre, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.

Manar A Alsaeedi (MA)

Neurology Department, Neuroscience Centre, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.

Raghad S Almuidh (RS)

Neurology Department, Neuroscience Centre, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.

Abdulbari A Alzahrani (AA)

Neurology Department, Neuroscience Centre, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.

Ahmad H Sakah (AH)

College of Medicine, Alfaisal University, Riyadh, Saudi Arabia.

Eman Mohamad El Nashar (EM)

Department of Anatomy, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Department of Histology and Cell Biology, Faculty of Medicine, Benha University, Benha, Egypt.

Mansour Y Otaif (MY)

Department of Pediatric, Neurology section, Abha Maternity and Childern Hospital, Abha, Saudi Arabia.

Nawal F Abdel Ghaffar (NF)

Neurology Department, Kasr Al Ainy Hospital, Faculty of Medicine, Cairo University, Giza, Egypt.
Neurology Department, Aseer Central Hospital, Abha, Saudi Arabia.

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Classifications MeSH