Abstract
Background: Numerous data show a role for genetic polymorphisms in the development of epilepsy. Previously, the TT genotype of the MTHFR 677C>T polymorphism was found to be associated with a decreased leucocyte DNA methylation status. Polymorphisms in the MTHFR gene could modify the pharmacodynamics of many drugs. This meta-analysis aimed to assess the relationship between MTHFR 677C>T polymorphism and susceptibility to epilepsy in young patients. Methods: Available databases (PubMed, Embase, Google Scholar, SciELO, and Medline) were searched using specific keywords. Eight studies, published between 1999 and 2019, with 1678 young patients with epilepsy and 1784 controls, met the inclusion criteria. Apart from the total groups, additional analyses in age subgroups (i.e., young adults and children) were conducted. Statistical analyses were conducted using the RevMan 5.4 and MedCalc software. The pooled odds ratio (OR) was estimated with a random- or fixed-effects model depending on the heterogeneity. Analyses were performed for five genetic models, i.e., dominant (CT + TT vs. CC), recessive (TT vs. CC + CT), additive (TT vs. CC), heterozygous (CT vs. CC), and allelic (T vs. C). The publication bias was assessed with the use of Egger’s and Begg’s tests. Results: Both the MTHFR TT genotype (in the additive model) and the T allele (in the allelic model) significantly increased the risk of epilepsy when the total groups were compared (OR = 1.44, p = 0.002, and OR = 1.183, p = 0.001, respectively). The sensitivity analysis for these models indicated the stability of the results. Similarly, significant results were obtained among young adults for all the genetic models (dominant model: OR = 1.28, p = 0.002; recessive model: OR = 1.48, p = 0.003; additive model: OR = 1.63, p < 0.001; heterozygous model: OR = 1.21, p = 0.028; and allelic model: OR = 1.256, p < 0.001). Those results were also stable and reliable. In the group of children, no relation between 677C>T polymorphism and epilepsy was observed; however, the analysis was based only on three studies, and one study also comprised young adults. No publication bias was demonstrated. Conclusions: The meta-analysis revealed that the carrier state for the T allele as well as the TT genotype of the MTHFR 677C>T polymorphism increases the risk of epilepsy in young adults but not in children.
Highlights
The pathogenesis of epilepsy, which is one of the most common neurological disorders worldwide, is heterogeneous but still not fully known
The meta-analysis revealed that the carrier state for the T allele as well as the TT genotype of the MTHFR 677C>T polymorphism increases the risk of epilepsy in young adults but not in children
The studies searched were included in the meta-analysis when the following criteria were met: (a) confirmed epilepsy, (b) patients and control groups, (c) ages of the patients younger than 45 years old, (d) access to data on genotypes, (e) full-length paper or brief communication, and (f) article written in English
Summary
The pathogenesis of epilepsy, which is one of the most common neurological disorders worldwide, is heterogeneous but still not fully known. In response to the damage factor within the latent period, the changes begin at the molecular level in gene expression and protein synthesis, and disturbances in the functioning of ion channels and neurons begin. The consequence of these changes is epileptic seizure as a clinical manifestation [1]. Neuroimaging recordings, seizures can be classified as focal, generalized and those of unknown onset. The common 677C>T polymorphism within the MTHFR gene was found to be related to the thermolability of the enzyme, which, in consequence, leads to an elevated level of homocysteine. The involvement of genes in the development of the disease may be of greater importance than in older patients
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