ArticleFrontiers in neurology2016
Promoter Variants of the ADAM10 Gene and Their Roles in Temporal Lobe Epilepsy.
Article in Frontiers in neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- The Contribution of Hippocampal All-Trans Retinoic Acid (ATRA) Deficiency to Alzheimer's Disease: A Narrative Overview of ATRA-Dependent Gene Expression in Post-Mortem Hippocampal Tissue.Antioxidants (Basel, Switzerland) · 2023Review
- Intercellular signaling by ectodomain shedding at the synapse.Trends in neurosciences · 2022Review
- Stage-dependent involvement of ADAM10 and its significance in epileptic seizures.Journal of cellular and molecular medicine · 2019Review
- Metalloprotease Adam10 suppresses epilepsy through repression of hippocampal neuroinflammation.Journal of neuroinflammation · 2018Article
- SRR intronic variation inhibits expression of its neighbouring SMG6 gene and protects against temporal lobe epilepsy.Journal of cellular and molecular medicine · 2018Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous evidence has indicated that downregulated ADAM10 gives rise to epileptic seizures in Alzheimer's disease, and this study investigated the association of ADAM10 with temporal lobe epilepsy (TLE) from a genetic perspective. A total of 496 TLE patients and 528 healthy individuals were enrolled and genotyped for ADAM10 promoter variants (rs653765 G > A and rs514049 A > C). The alleles, genotypes, and haplotypes were then compared with clarify the association of these variants with TLE and their impacts upon age at onset, initial seizure types before treatments, and responses to drug treatments. In cohorts I, II, and I + II, the frequencies of the A allele and AA genotype at rs514049 were consistently increased in the cases compared with the controls (p = 0.020 and p = 0.009; p = 0.008 and p = 0.009; p = 0.000 and p = 0.000; q = 0.003 and q = 0.002, respectively). In contrast, the frequency of the AC haplotype (rs653765-rs514049) decreased in cohorts I + II (p = 0.013). Further analyses of the TLE patients indicated that the AA genotype functioned as a predisposing factor to drug-resistant TLE and the AC haplotype as a protective factor against generalized tonic-clonic seizures (GTCS) and drug-resistant TLE. This study is the first to demonstrate an association of the ADAM10 promoter variants with TLE. In particular, the AA genotype and AC haplotype showed their effects upon GTCS and drug-resistant TLE.
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