Differential DNA Methylation Profiles in Patients with Temporal Lobe Epilepsy and Hippocampal Sclerosis ILAE Type I

Zhang, Wang; Wang, Haiyang; Liu, Binchao; Jiang, Miaomiao; Gu, Yifei; Shi, Yan; Han, Xian; Karachi, Aida; Tang, Chongyang; Jiang, Zhenfeng; Shen, Hong; Meng, Na; Lin, Zhiguo

doi:10.1007/s12031-020-01780-9

Cited by 17 publications

(10 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The link between hypermethylation and epileptogenesis hypothesis thus proposed states that increased DNMT activity and resultant global genomic hypermethylation that may lead to the progression of the disease as well as maintenance of the diseased state in an affected individual [ 46 ]. Interestingly, recent whole genome bisulfite sequencing (WGBS) of the DNA samples collected from relevant patients suffering from TLE-HS type I and TLE without HS, revealed 1171 hypermethylated and 2537 hypomethylated regions, in addition to 632 differentially methylated genes that are primarily involved in epileptogenesis [ 97 ]. This further underlined the critical role of DNA methylation as an imperative factor regulating the onset and sub-type of this disease.…”

Section: Maternal Dietary and Supplementary Intakesmentioning

confidence: 99%

DNA methylation and regulation of gene expression: Guardian of our health

Dhar

Saha

Mitra

et al. 2021

Nucleus

119

View full text Add to dashboard Cite

One of the most critical epigenetic signatures present in the genome of higher eukaryotes is the methylation of DNA at the C-5 position of the cytosine ring. Based on the sites of DNA methylation in a locus, it can serve as a repressive or activation mark for gene expression. In a crosstalk with histone modifiers, DNA methylation can consequently either inhibit binding of the transcription machinery or generate a landscape conducive for transcription. During developmental phases, the DNA methylation pattern in the genome undergoes alterations as a result of regulated balance between de novo DNA methylation and demethylation. Resultantly, differentiated cells inherit a unique DNA methylation pattern that fine tunes tissue-specific gene expression. Although apparently a stable epigenetic mark, DNA methylation is actually labile and is a complex reflection of interaction between epigenome, genome and environmental factors prior to birth and during progression of life. Recent findings indicate that levels of DNA methylation in an individual is a dynamic outcome, strongly influenced by the dietary environment during germ cell formation, embryogenesis and post birth exposures. Loss of balances in DNA methylation during developmental stages may result in imprinting disorders, while at any later stage may lead to increased predisposition to various diseases and abnormalities. This review aims to provide an outline of how our epigenome is uniquely guided by our lifetime of experiences beginning in the womb and how understanding it better holds future possibilities of improvised clinical applications.

show abstract

Section: Maternal Dietary and Supplementary Intakesmentioning

confidence: 99%

DNA methylation and regulation of gene expression: Guardian of our health

Dhar

Saha

Mitra

et al. 2021

Nucleus

119

View full text Add to dashboard Cite

show abstract

“…As for cfDNA methylation, nothing has, to the best of our knowledge, been reported yet. Nonetheless, altered DNA methylation patterns in brain tissue of epilepsy patients have been consistently described (Miller-Delaney et al, 2012 ; Liu et al, 2016 ; Wang et al, 2016 ; Zhang et al, 2021 ; Martins-Ferreira et al, 2022 ). Major efforts have been made for the use of DNA methylation as peripheral biomarkers, namely by demonstrating the correlation of DNA methylation patterns in brain tissue and peripheral tissues, such as blood, saliva, and buccal mucosa (Braun et al, 2019 ).…”

Section: Potential Of Cfdna Methylome Profiling In Epilepsymentioning

confidence: 99%

The Potential of Circulating Cell-Free DNA Methylation as an Epilepsy Biomarker

Martins-Ferreira

Leal

Costa

2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Circulating cell-free DNA (cfDNA) are highly degraded DNA fragments shed into the bloodstream. Apoptosis is likely to be the main source of cfDNA due to the matching sizes of cfDNA and apoptotic DNA cleavage fragments. The study of cfDNA in liquid biopsies has served clinical research greatly. Genetic analysis of these circulating fragments has been used in non-invasive prenatal testing, detection of graft rejection in organ transplants, and cancer detection and monitoring. cfDNA sequencing is, however, of limited value in settings in which genetic association is not well-established, such as most neurodegenerative diseases.Recent studies have taken advantage of the cell-type specificity of DNA methylation to determine the tissue of origin, thus detecting ongoing cell death taking place in specific body compartments. Such an approach is yet to be developed in the context of epilepsy research. In this article, we review the different approaches that have been used to monitor cell-type specific death through DNA methylation analysis, and recent data detecting neuronal death in neuropathological settings. We focus on the potential relevance of these tools in focal epilepsies, like Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis (MTLE-HS), characterized by severe neuronal loss. We speculate on the potential relevance of cfDNA methylation screening for the detection of neuronal cell death in individuals with high risk of epileptogenesis that would benefit from early diagnosis and consequent early treatment.

show abstract

“…Aside from gene-specific changes in DNA methylation, altered global DNA methylation has also been reported in epilepsy. Differences in DNA methylation profiles have been reported between brain tissue samples collected from patients with temporal lobe epilepsy-hippocampal sclerosis ILAE Type I compared to temporal lobe epilepsy with non-hippocampal sclerosis using whole-genome bisulfite sequencing [103]. The study identified potential cellular signaling pathways associated with differentially methylated regions at the whole-genome level, as well as in the context of promoter regions [103].…”

Section: Atrx Chd2 Ehmt1 Kansl1 Kdm5c Whs Cnvsmentioning

confidence: 99%

Complexity in Genetic Epilepsies: A Comprehensive Review

Rastin,

Schenkel,

Sadikovic

2023

IJMS

View full text Add to dashboard Cite

Epilepsy is a highly prevalent neurological disorder, affecting between 5–8 per 1000 individuals and is associated with a lifetime risk of up to 3%. In addition to high incidence, epilepsy is a highly heterogeneous disorder, with variation including, but not limited to the following: severity, age of onset, type of seizure, developmental delay, drug responsiveness, and other comorbidities. Variable phenotypes are reflected in a range of etiologies including genetic, infectious, metabolic, immune, acquired/structural (resulting from, for example, a severe head injury or stroke), or idiopathic. This review will focus specifically on epilepsies with a genetic cause, genetic testing, and biomarkers in epilepsy.

show abstract

Differential DNA Methylation Profiles in Patients with Temporal Lobe Epilepsy and Hippocampal Sclerosis ILAE Type I

Cited by 17 publications

References 40 publications

DNA methylation and regulation of gene expression: Guardian of our health

DNA methylation and regulation of gene expression: Guardian of our health

The Potential of Circulating Cell-Free DNA Methylation as an Epilepsy Biomarker

Complexity in Genetic Epilepsies: A Comprehensive Review

Contact Info

Product

Resources

About