Non-Coding RNAs: New Biomarkers and Therapeutic Targets for Temporal Lobe Epilepsy

Manna, Ida; Fortunato, Francesco; Benedittis, Selene De; Sammarra, Ilaria; Bertoli, Gloria; Labate, Angelo; Gambardella, Antonio

doi:10.3390/ijms23063063

Cited by 16 publications

(7 citation statements)

References 102 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mechanisms likely differ based on injury type and location but involve astrocyte activation, mTOR signaling, inflammation, glial activation, and cell communication (Table 1). Analyses of human and animal tissues and transcriptomic and proteomic analyses have revealed molecular networks and noncoding RNAs involved 28 . However, the complexity of interactions makes antiepileptogenic drug development challenging.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Advances in understanding the pathogenesis of epilepsy: Unraveling the molecular mechanisms

Shariff,

Nouh,

Inshutiyimana

et al. 2024

Health Science Reports

View full text Add to dashboard Cite

IntroductionEpilepsy is characterized by having two or more unprovoked seizures. Understanding the pathogenesis of epilepsy, requires deep investigation into the molecular mechanisms. This helps develop diagnostic techniques, treatments, and pharmacotherapy. It also enhances precision medicine and individualized treatment processes. This article reviews all the molecular mechanisms predisposing to epileptogenesis, presents the current diagnostic techniques and drug therapy, and suggests future perspectives in treating Epilepsy in a more comprehensive and holistic approach.MethodologyFour authors searched keywords concerning epilepsy at a molecular level, Epilepsy diagnostic techniques and technologies, and antiepileptic drug therapy and precision medicine. Separate search strategies were conducted for each concern and retrieved articles were reviewed for relevant results.ResultsThe traditional diagnostic techniques for Epilepsy and its pathogenesis are insufficient in highlighting dynamic brain changes. For this, emerging technologies including genetic sequencing and profiling, and functional neuroimaging techniques are prevailing. Concerning treatment, the current approach focuses on managing symptoms and stopping seizures using antiseizure medications. However, their usage is limited by developing resistance to such drugs. Some therapies show promise, although most antiseizure drugs do not prevent epilepsy.DiscussionUnderstanding epileptogenesis at a molecular and genetic level aids in developing new antiepileptic pharmacotherapy. The aim is to develop therapies that could prevent seizures or modify disease course, decreasing the severity and avoiding drug resistance. Gene therapy and precision medicine are promising but applications are limited due to the heterogeneity in studying the Epileptic brain, dynamically. The dynamic investigation of the epileptic brain with its comorbidities works hand‐in‐hand with precision medicine, in developing personalized treatment plans.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Analyses of human and animal tissues and transcriptomic and proteomic analyses have revealed molecular networks and noncoding RNAs involved. 28 However, the complexity of interactions makes antiepileptogenic drug development challenging. Beyond drugs, gene and cell therapies may provide targeted disease modification.…”

Section: Discussionmentioning

confidence: 99%

Advances in understanding the pathogenesis of epilepsy: Unraveling the molecular mechanisms

Shariff,

Nouh,

Inshutiyimana

et al. 2024

Health Science Reports

View full text Add to dashboard Cite

show abstract

“…Apoptosis, inflammation, and pathological circuit re-formation are other mechanisms contribute to the pathophysiology of epilepsy, in which miRNAs might be involved. 10 , 11 , 33 Brain injury in patients with epilepsy can promote the release of inflammatory factors and induce inflammatory reactions. These inflammatory factors (e.g., IL-1, INF-α, and TNF-α) can destroy the blood–brain barrier and aggravate damage to the nervous system and also excite neurons and promote repeated seizures.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of MicroRNAs in Pediatric Epilepsy

Çarman¹,

Tekin²,

Çavuşoğlu³

et al. 2023

Turkish Archives of Pediatrics

View full text Add to dashboard Cite

Objective: The pathophysiology of epilepsy remains unknown. Recent research has shown that microRNA expression changes in epileptic adults. In the present work, we aimed to identify serum microRNA expression in drug-responsive and resistant children with idiopathic generalized epilepsy. Materials and Methods: The study included 43 (20 male and 23 female) epilepsy patients and 66 (43 male and 23 female) control subjects. The mean ages of the groups were 113.41 ± 61.83 and 105.46 ± 62.31 months, respectively. Twenty-eight epileptic patients were classified as drug resistant. Thirteen of the controls were the siblings of patients with epilepsy. The study only included children with idiopathic generalized epilepsy who had normal brain magnetic resonance imaging. The serum microRNA expressions (microRNA-181a, microRNA-155, microRNA-146, and microRNA-223) were investigated. Expressions of serum microRNA-181a, microRNA-155, microRNA-146, and microRNA-223 were previously investigated in epilepsy patients and children with febrile seizures. Therefore, these microRNAs were chosen. The expressions of serum levels of microRNAs were determined using quantitative real-time polymerase chain reaction. Results: The results indicated that the expressions of serum microRNA-155 and microRNA-223 were elevated in epileptic children ( P < .05). The expression of the same microRNAs was also elevated in individuals with drug-resistant epilepsy compared to healthy controls ( P < .05). microRNA-146a, microRNA-155, and microRNA-223 expressions were higher in drug-resistant patients than in drug-responsive children ( P < .05). A logistic regression study determined that an increase of microRNA-155 was a risk for epilepsy, while a decrease of microRNA-146a risk for epilepsy. Conclusion: Few researchers have investigated the function of microRNAs in the development of childhood epilepsy. Our findings revealed that epilepsy patients have abnormal microRNAexpression.

show abstract

“…These epigenetic factors regulate the pathophysiological process of epilepsy and have been found to be dysregulated during epileptogenesis. Experiments in human subjects affected with epilepsy and in animal models of this disorder have shown abnormal expression of non-coding RNAs ( Manna et al, 2022 ). Based on the importance of lncRNAs in the regulation of Treg functions ( Luo and Wang, 2020 ), we have selected five Treg-related lncRNAs to assess their expression in patients with epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Assessment of Treg-related lncRNAs in epilepsy

Sharifi

Eghtedarian²,

Taheri³

et al. 2023

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Recent studies have shown dysregulation of several groups of long non-coding RNAs in the context of epilepsy. According to evidence regarding the role of regulatory T cells in this disorder, we examined expression levels of regulatory T cell-related lncRNAs, namely TH2-LCR, RMRP, IFNG-AS1 (NEST), MAFTRR and FLICR in the blood of epileptic cases compared with controls. Expression of RMRP was lower in patients with refractory epilepsy compared with controls [expression ratio (95% CI) = 0.32 (0.13–0.8), adjusted p-value = 0.0008]. Besides, its expression was lower in refractory patients vs. non-refractory patients [expression ratio (95% CI) = 0.2 (0.1–0.41), adjusted p-value < 0.0001]. Expression of TH2-LCR was lower in refractory patients vs. controls [expression ratio (95% CI) = 0.4 (0.17–0.93), adjusted p-value = 0.0044] and in refractory patients vs. non-refractory ones [Expression ratio = 0.28 (0.19–0.58), p-value < 0.0001]. Expression of NEST was higher in total patients [expression ratio (95% CI) = 2.48 (1.15–5.27), adjusted p-value = 0.0012] and in both groups of patients compared with controls. However, its expression was not different between refractory and non-refractory cases. Similarly, FLICR and MAFTRR were over-expressed in total cases and both groups of patients compared with controls, but their expressions were similar between refractory and non-refractory cases. MAFTRR could differentiate between total epileptic cases and controls with AUC value of 0.8. This lncRNA could separate refractory and non-refractory cases from healthy controls with AUC values of 0.73 and 0.88, respectively. This study provides evidence for deregulation of regulatory T cell-related lncRNAs in epilepsy and their potential role as diagnostic markers in this condition.

show abstract

Non-Coding RNAs: New Biomarkers and Therapeutic Targets for Temporal Lobe Epilepsy

Cited by 16 publications

References 102 publications

Advances in understanding the pathogenesis of epilepsy: Unraveling the molecular mechanisms

Advances in understanding the pathogenesis of epilepsy: Unraveling the molecular mechanisms

Evaluation of MicroRNAs in Pediatric Epilepsy

Assessment of Treg-related lncRNAs in epilepsy

Contact Info

Product

Resources

About