Correlation between synaptic protein expression and synaptic reorganization in the hippocampal CA3 region in a rat model of post-traumatic epilepsy

Postsynaptic density protein-95 and synaptophysin participate in synaptic reorganization in the forebrain of epilepsy models. However, the time-effect relationship between dynamic synapsin expression in hippocampus and synaptic reorganization in the post-traumatic epilepsy model remains unclear. FeCI2 was injected into the hippocampal CA3 region of the right forebrain in rats to induce post-traumatic epilepsy. Postsynaptic density protein-95 and synaptophysin expression was detected using immunohistochemistry. Epileptiform discharge induced by FeCI2 injection was determined in rat forebrain neurons, revealing decreased postsynaptic density protein-95 expression at 24 hours and lowest levels at 7 days. Synaptophysin expression was markedly reduced at 24 hours, but increased at 7 days. Postsynaptic density protein-95 and synaptophysin expression was consistent with abnormal mossy fiber sprouting and synaptic reorganization following neuronal injury in the hippocampal CA3 region of FeCI2-induced epilepsy models.

Synaptic plasticity effects on FeCl_2-induced post-traumatic epilepsy onset in the rat

Studies have confirmed that iron induces epilepsy onset, and iron ion-induced epilepsy in anima models closely resembles the clinical situation. Models of post-traumatic epilepsy （PTE） were established by intracortical injection of FeCl2 using stereotactic techniques. Electron microscopy revealed neuronal degeneration, with shrinkage of the neuronal soma, hyperplasia of rough endoplasmic reticulum, ribosomal detachment from the endoplasmic reticulum, and vacuolar degeneration of glial cells in the right frontal lobe of FeCl2-induced PTE rats. With prolonged time injuries became more severe and neuronal apoptosis was observed. Synapses in the hippocampal neuropil significantly increased （primarily type I/excitatory synapses） at day 14 following injury. Type II synapses （inhibitory synapse） were observed in the rat hippocampus at day 30. Cortical neuronal degeneration, apoptosis, glial cell proliferation, and ultrastructural hippocampal changes, in particular changes in type of neuronal synapse, play an important role in PTE onset.

MicroRNAs as potential biomarkers for diagnosis of post-traumatic stress disorder

Post-traumatic stress disorder is a mental disorder caused by exposure to severe traumatic life events.Currently,there are no validated biomarkers or laboratory tests that can distinguish between trauma survivors with and without post-traumatic stress disorder.In addition,the heterogeneity of clinical presentations of post-traumatic stress disorder and the overlap of symptoms with other conditions can lead to misdiagnosis and inappropriate treatment.Evidence suggests that this condition is a multisystem disorder that affects many biological systems,raising the possibility that peripheral markers of disease may be used to diagnose post-traumatic stress disorder.We performed a PubMed search for microRNAs(miRNAs)in post-traumatic stress disorder(PTSD)that could serve as diagnostic biomarkers and found 18 original research articles on studies performed with human patients and published January 2012 to December 2023.These included four studies with whole blood,seven with peripheral blood mononuclear cells,four with plasma extracellular vesicles/exosomes,and one with serum exosomes.One of these studies had also used whole plasma.Two studies were excluded as they did not involve microRNA biomarkers.Most of the studies had collected samples from adult male Veterans who had returned from deployment and been exposed to combat,and only two were from recently traumatized adult subjects.In measuring miRNA expression levels,many of the studies had used microarray miRNA analysis,miRNA Seq analysis,or NanoString panels.Only six studies had used real time polymerase chain reaction assay to determine/validate miRNA expression in PTSD subjects compared to controls.The miRNAs that were found/validated in these studies may be considered as potential candidate biomarkers for PTSD and include miR-3130-5p in whole blood;miR-193a-5p,-7113-5p,-125a,-181c,and-671-5p in peripheral blood mononuclear cells;miR-10b-5p,-203a-3p,-4488,-502-3p,-874-3p,-5100,and-7641 in plasma extracellular vesicles/exosomes;and miR-18a-3p and-7-1-5p in blood plasma.Several important limitations identified in the studies need to be taken into account in future studies.Further studies are warranted with war veterans and recently traumatized children,adolescents,and adults having PTSD and use of animal models subjected to various stressors and the effects of suppressing or overexpressing specific microRNAs.

Pathogenesis, diagnosis, and treatment of epilepsy: electromagnetic stimulation-mediated neuromodulation therapy and new technologies

Epilepsy is a severe,relapsing,and multifactorial neurological disorder.Studies regarding the accurate diagnosis,prognosis,and in-depth pathogenesis are crucial for the precise and effective treatment of epilepsy.The pathogenesis of epilepsy is complex and involves alterations in variables such as gene expression,protein expression,ion channel activity,energy metabolites,and gut microbiota composition.Satisfactory results are lacking for conventional treatments for epilepsy.Surgical resection of lesions,drug therapy,and non-drug interventions are mainly used in clinical practice to treat pain associated with epilepsy.Non-pharmacological treatments,such as a ketogenic diet,gene therapy for nerve regeneration,and neural regulation,are currently areas of research focus.This review provides a comprehensive overview of the pathogenesis,diagnostic methods,and treatments of epilepsy.It also elaborates on the theoretical basis,treatment modes,and effects of invasive nerve stimulation in neurotherapy,including percutaneous vagus nerve stimulation,deep brain electrical stimulation,repetitive nerve electrical stimulation,in addition to non-invasive transcranial magnetic stimulation and transcranial direct current stimulation.Numerous studies have shown that electromagnetic stimulation-mediated neuromodulation therapy can markedly improve neurological function and reduce the frequency of epileptic seizures.Additionally,many new technologies for the diagnosis and treatment of epilepsy are being explored.However,current research is mainly focused on analyzing patients’clinical manifestations and exploring relevant diagnostic and treatment methods to study the pathogenesis at a molecular level,which has led to a lack of consensus regarding the mechanisms related to the disease.

The role of axon guidance molecules in the pathogenesis of epilepsy

Current treatments for epilepsy can only manage the symptoms of the condition but cannot alter the initial onset or halt the progression of the disease. Consequently, it is crucial to identify drugs that can target novel cellular and molecular mechanisms and mechanisms of action. Increasing evidence suggests that axon guidance molecules play a role in the structural and functional modifications of neural networks and that the dysregulation of these molecules is associated with epilepsy susceptibility. In this review, we discuss the essential role of axon guidance molecules in neuronal activity in patients with epilepsy as well as the impact of these molecules on synaptic plasticity and brain tissue remodeling. Furthermore, we examine the relationship between axon guidance molecules and neuroinflammation, as well as the structural changes in specific brain regions that contribute to the development of epilepsy. Ample evidence indicates that axon guidance molecules, including semaphorins and ephrins, play a fundamental role in guiding axon growth and the establishment of synaptic connections. Deviations in their expression or function can disrupt neuronal connections, ultimately leading to epileptic seizures. The remodeling of neural networks is a significant characteristic of epilepsy, with axon guidance molecules playing a role in the dynamic reorganization of neural circuits. This, in turn, affects synapse formation and elimination. Dysregulation of these molecules can upset the delicate balance between excitation and inhibition within a neural network, thereby increasing the risk of overexcitation and the development of epilepsy. Inflammatory signals can regulate the expression and function of axon guidance molecules, thus influencing axonal growth, axon orientation, and synaptic plasticity. The dysregulation of neuroinflammation can intensify neuronal dysfunction and contribute to the occurrence of epilepsy. This review delves into the mechanisms associated with the pathogenicity of axon guidance molecules in epilepsy, offering a valuable reference for the exploration of therapeutic targets and presenting a fresh perspective on treatment strategies for this condition.

Exploring cerebral structural and functional abnormalities in a mouse model of post-traumatic headache induced by mild traumatic brain injury

Mild traumatic brain injury(mTBI)-induced post-traumatic headache(PTH)is a pressing public health concern and leading cause of disability worldwide.Although PTH is often accompanied by neurological disorders,the exact underlying mechanism remains largely unknown.Identifying potential biomarkers may prompt the diagnosis and development of effective treatments for mTBI-induced PTH.In this study,a mouse model of mTBI-induced PTH was established to investigate its effects on cerebral structure and function during short-term recovery.Results indicated that mice with mTBI-induced PTH exhibited balance deficits during the early post-injury stage.Metabolic kinetics revealed that variations in neurotransmitters were most prominent in the cerebellum,temporal lobe/cortex,and hippocampal regions during the early stages of PTH.Additionally,variations in brain functional activities and connectivity were further detected in the early stage of PTH,particularly in the cerebellum and temporal cortex,suggesting that these regions play central roles in the mechanism underlying PTH.Moreover,our results suggested that GABA and glutamate may serve as potential diagnostic or prognostic biomarkers for PTH.Future studies should explore the specific neural circuits involved in the regulation of PTH by the cerebellum and temporal cortex,with these two regions potentially utilized as targets for non-invasive stimulation in future clinical treatment.

Promoting Post-Traumatic Growth in Colorectal Cancer Patients:Exploring the Role of Social Support through a Chain Mediation Model

Colorectal cancer(CRC)poses significant physical and psychological challenges that necessitate an exploration of factors influencing post-traumatic growth(PTG)for patient well-being.This study aims to investigate the effects of positive psychological capital(PsyCap)and perceived stress on mediating the social support-PTG relation among 673 CRC patients.Social support,positive PsyCap,perceived stress,and PTG were assessed through questionnaires.The results indicated a direct prediction effect of social support on PTG(LICI=0.481,ULCI=0.644),with the direct effect being 59.5%.Both positive PsyCap and perceived stress exerted a mediating role in the correlation between social support and PTG,with the mediating effects occupying 29.4%(LICI=0.217,ULCI=0.343)and 5.7%(LICI=0.030,ULCI=0.082),respectively.Positive PsyCap further had a chain mediating effect on perceived stress(LICI=0.031,ULCI=0.074),with the chain effect accounting for 5.4%.The total impact of social support on PTG was 100%(LICI=0.882,ULCI=1.008).This model underscores the pivotal role of social support in promoting PTG in CRC patients.Positive PsyCap serves as a crucial mediator in the social support-PTG link,with perceived stress playing a sequential mediating role.Thesefindings suggest that strengthening social support networks and cultivating positive PsyCap may reduce perceived stress and promote the development of PTG in CRC patients.Consequently,intervention programs are recommended to improve the psychosocial well-being of CRC patients.

Ginger oil-loaded transdermal adhesive patch treats post-traumatic stress disorder

Objective:To find a viable alternative to reduce the number of doses required for the patients with post-traumatic stress disorder(PTSD),and to improve efficacy and patient compliance.Methods: In this study,we used ginger oil,a phytochemical with potential therapeutic properties,to prepare ginger oil patches.High-performance liquid chromatography(HPLC)was used to quantify the main active component of ginger oil,6-gingerol.Transdermal absorption experiments were conducted to optimize the various pressure-sensitive adhesives and permeation enhancers,including their type and concentration.Subsequently,the ginger oil patches were optimized and subjected to content determination and property evaluations.A PTSD mouse model was established using the foot-shock method.The therapeutic effect of ginger oil patches on PTSD was assessed through pathological sections,behavioral tests,and the evaluation of biomarkers such as tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),brain-derived neurotrophic factor(BDNF),and melatonin(MT).Results: The results demonstrated that ginger oil patches exerted therapeutic effects against PTSD by inhibiting inflammatory responses and modulating MT and BDNF levels.Pharmacokinetic experiments revealed that ginger oil patches maintained a stable blood drug concentration for at least one day,addressing the rapid metabolism drawback of 6-gingerol and enhancing its therapeutic efficacy.Conclusions: Ginger oil can be prepared as a transdermal drug patch that meets these requirements,and the bioavailability of the prepared patch is better than that of oral administration.It can improve PTSD with good patient compliance and ease of administration.Therefore,it is a promising therapeutic formulation for the treatment of PTSD.

Effects of Pearl Yangxin Anshen Decoction on HAMD and PTSD-SS Scores, Cytokines and Related Metabolites in Patients with Post-Traumatic Stress Disorder

Objective: This paper aims to observe the Pearl Yangxin Anshen Decoction to influence the score of HAMD and PTSD-SS, the changes of the cytokines and the related metabolic product in patients with PTSD. Methods: From June 2015 to May 2016, in the traditional Chinese medicine clinics of Hainan Province People’s Hospital, there were 50 patients with PTSD, the age were from 30 to 60, they were randomly divided into treatment group (25 cases) and control group (25 cases), then compared the scores of HAMD and PTSD-SS between the two groups, searched the changes of cytokines and the related metabolic product. Results: In the treatment group: before and after treatment the scores of PTSD-SS were 65.64 ± 7.02, 28.32 ± 4.18, and the scores of HAMD were 29.28 ± 1.97, 11.72 ± 2.13;In the control group: before and after treatment the scores of PTSD-SS were 63.24 ± 6.16, 31.40 ± 4.29, the scores of HAMD were 30.24 ± 2.05, 13.08 ± 2.30. After 3 months patients in treatment group the scores of PTSD-SS and HAMD were lower than the control group (t = 2.570, P = 0.013, t = -2.1640, P = 0.035). In the control group: before and after 3 months treatment the IL-2 levels respectively were 79.84 ± 26.46 pg/ml, 56.18 ± 22.67 pg/ml, the IL-6 levels respectively were 110.83 ± 47.65 pg/ml, 59.67 ± 44.68 pg/ml, the IL-8 levels respectively were 73.11 ± 78.51 pg/ml, 55.83 ± 81.94 pg/ml, the NE levels respectively were 420.04 ± 674.75 pg/ml, 185.31 ± 417.91 pg/ml, the MDA levels respectively were 112.35 ± 62.87 ng/ml, 60.42.33 ± 53.64 ng/ml, the NO levels were 126.6 ± 47.4 μmol/L, 78.6 ± 45.7 μmol/L, the VIP levels were 396.6 ± 144.4 pg/ml, 122.4 ± 111.5 pg/ml. In the treatment group: before and after 3 months treatment the IL-2 levels respectively were 86.00 ± 32.29 pg/ml, 53.84 ± 27.01 pg/ml, the IL-6 levels respectively were 108.21 ± 44.60 pg/ml, 42.46 ± 42.16 pg/ml, the IL-8 levels respectively were 81.48 ± 94.19 pg/ml, 54.07 ± 84.15 pg/ml, the NE levels respectively were 392.93 ± 592.84 pg/ml, 243.85 ± 588.45 pg/ml, the MDA levels respectively were 117.58 ± 63.37 ng/ml, 45.91 ± 38.94 ng/ml, the NO levels respectively were 135.9 ± 46.4 μmol/L, 72.6 ± 46.6 μmol/L, the VIP levels respectively were 414.0 ± 140.1 pg/ml, 185.8 ± 105.3 pg/ml. In the two groups as the extension of treatment time, the content of IL-2, IL-8, IL-6, NE, MDA, NO, and VIP were gradually reduced, and the level of reduction of the treatment group patients was higher than the control group, the change of ACTH and SOD levels just the opposite. Conclusion: The Pearl Yangxin Anshen Decoction could improve the symptoms of psychological anxiety, depression and other psychological problems in patients with PTSD, and influence the change of cytokines and related metabolites product.

Correlation Study of Neurotransmitter and Immune Levels in Pre-Hospital Emergency Nurses with Post-Traumatic Stress Disorder

Objective: To investigate the occurrence of PTSD in pre-hospital emergency nurses and its related factors, and to compare the differences of neurotransmitter and immune-related factors between pre-hospital emergency nurses who experienced traumatic events and those who did not develop PTSD and healthy people. How: Post-traumatic Stress Disorder Self-Rating Scale (PCL-C) tests were performed on pre-hospital emergency nurses in PTSD group, non-PTSD group and healthy control group, and the plasma monoamine neurotransmitters and serum cytokines were determined by double-antibody sandwich ABC-ELISA assay using enzyme-linked adsorption kit provided by Shanghai Xitang Biotechnology Co., Ltd. Results: 1) There were statistically significant differences in PCL-C scores between PTSD group, non-PTSD group and healthy group (p α between PTSD group, non-PTSD group and healthy group (p Conclusion: Pre-hospital emergency nurses should have early psychological intervention and guidance to reduce the occurrence of PTSD in emergency and emergency nurses.

Principles and Techniques of Post-Traumatic Rhinoplasty: A Review of the Literature

Post-traumatic rhinoplasty is the surgical treatment of the complex functional and aesthetic sequelae of nasal trauma. Correcting a post-traumatic nose is a challenging task, requiring the surgeon to employ a range of techniques and grafts to adequately address the deformities observed. The results of our research show that restoring pre-traumatic form and function remains complex, although many guidelines have been established to refine and optimize the management of the after-effects of nasal trauma. But it is achievable with the right techniques. The objective of our review is to highlight the various post-traumatic nasal sequelae, describe the fundamental principles in the field of post-traumatic rhinoplasty and provide the surgeon with the various existing surgical techniques and strategies so that he or she can make an appropriate choice for the patient.

Quality of life and its influencing factors in patients with post-traumatic epilepsy

Objective： To observe the quality of life in patients with post-traumatic epilepsy and discuss the infuencing factors. Methods： We assessed 105 patients with post-traumatic epilepsy and 100 healthy people as control using Quality of Life Scale-31 （QOL-31）, Self-rating Depressing Scale （SDS） and Self-rating Anxiety Scale （SAS）, and conducted retrospective analysis on the depression, anxiety, site of trauma, control of seizure, EEG and therapeutic compliance. Results： Patients with post-traumatic epilepsy scored much lower than the control group on QOL-31 （P〈0.01）, but higher than the control group on SDS and SAS （P〈0.01）. Multiple regression analysis indicated that major influencing factors on the quality of life were anxiety, therapeutic compliance, depression, poor control of epileptic seizure and site of trauma. Conclusions： The quality of life in patients with posttraumatic epilepsy has significantly declined. Doctors should pay attention to psychological and mental problems of patients with epilepsy, such as depression and anxiety, enhancing therapeutic compliance and controlling epileptic seizure, which are the keys to improving prognosis.

Elevated NKCC1 transporter expression facilitates early post-traumatic brain injury seizures

As a leading cause for morbidity and mortality in young adults,traumatic brain injury（TBI）,along with the poorly understood TBI-related seizures inducing their predispositions,pose a major health and socioeconomic problem in the world（Huang,2013）.

Treadmill exercise improves hippocampal neural plasticity and relieves cognitive deficits in a mouse model of epilepsy

Epilepsy frequently leads to cognitive dysfunction and approaches to treatment remain limited.Although regular exercise effectively improves learning and memory functions across multiple neurological diseases,its application in patients with epilepsy remains controversial.Here,we adopted a 14-day treadmill-exercise paradigm in a pilocarpine injection-induced mouse model of epilepsy.Cognitive assays confirmed the improvement of object and spatial memory after endurance training,and electrophysiological studies revealed the maintenance of hippocampal plasticity as a result of physical exercise.Investigations of the mechanisms underlying this effect revealed that exercise protected parvalbumin interneurons,probably via the suppression of neuroinflammation and improved integrity of blood-brain barrier.In summary,this work identified a previously unknown mechanism through which exercise improves cognitive rehabilitation in epilepsy.

Flexible,high-density,laminated ECoG electrode array for high spatiotemporal resolution foci diagnostic localization of refractory epilepsy

High spatiotemporal resolution brain electrical signals are critical for basic neuroscience research and high-precision focus diagnostic localization,as the spatial scale of some pathologic signals is at the submillimeter or micrometer level.This entails connecting hundreds or thousands of electrode wires on a limited surface.This study reported a class of flexible,ultrathin,highdensity electrocorticogram(ECoG)electrode arrays.The challenge of a large number of wiring arrangements was overcome by a laminated structure design and processing technology improvement.The flexible,ultrathin,high-density ECoG electrode array was conformably attached to the cortex for reliable,high spatial resolution electrophysiologic recordings.The minimum spacing between electrodes was 15μm,comparable to the diameter of a single neuron.Eight hundred electrodes were prepared with an electrode density of 4444 mm^(-2).In focal epilepsy surgery,the flexible,high-density,laminated ECoG electrode array with 36 electrodes was applied to collect epileptic spike waves inrabbits,improving the positioning accuracy of epilepsy lesions from the centimeter to the submillimeter level.The flexible,high-density,laminated ECoG electrode array has potential clinical applications in intractable epilepsy and other neurologic diseases requiring high-precision electroencephalogram acquisition.

How to establish an expected animal model of post-traumatic osteoarthritis?

Background：Animal models of osteoarthritis（OA）,including post-traumatic osteoarthritis and spontaneous osteoarthritis,have been established in many ways.In recent years,there have been many reports in various foreign academic journals,but animal models of post-traumatic osteoarthritis（distinct from spontaneous osteoarthritis） have rarely been established or summarized in these reports.Animal models of post-traumatic osteoarthritis show different characteristics depending on the animal species and modeling methods used,which is why we have written this article.Objective：To summarize the research progress and research status of animal models of post-traumatic osteoarthritis.Methods：A retrospective review of the animal model of post-traumatic osteoarthritis（OA） was conducted on the basis of reports retrieved from the PubMed database with the keywords for searching ＂animal model,post-traumatic osteoarthritis（PTOA）＂ from October 2006 to October 2016 and confided English language.A total of 80 academic articles on the study of animal models of traumatic osteoarthritis were retrieved,and 34 of them were included in this literature review after reading the free fulltext of them.Results：Different PTOA models based on different modeling methods and different animal species had their own characteristics.Different modeling methods should be selected according to different modeling animals.Conclusions：Considering the project funds,experimental objectives and technical conditions,appropriate experimental animal and modeling method should be selected based on synthetic considerations to obtain an appropriate PTOA model and ideal experimental results.

Aberrant adult neurogenesis in intractable epilepsy:can GABAergic progenitor transplantation normalize this process?

Temporal lobe epilepsy(TLE) is a common type of focal epilepsy characterized by seizure foci within the temporal lobes.While surgical resection of the foci is an established and effective approach for controlling seizures,both temporal lobes cannot be removed,due to their prominent roles in learning and memory.Additionally,seizures induce changes to the temporal lobes that contribute to hyperexcitability,including mossy fiber sprouting,astrogliosis.

Astrocyte chloride,excitatory-inhibitory balance and epilepsy

Excitation and inhibition are at the core of brain function and malfunction.To sustain the activity of neuronal networks over time and space,glutamatergic excitation is balanced by GABAergic inhibition.The equipoise of excitation and inhibition,known as the excitation/inhibition(E/I)balance,is crucial for proper brain function.The E/I balance is highly dynamic and shifts across different brain states:wakefulness primarily augments excitatory activity,while sleep promotes a decrease in excitation and an increase in inhibition(Bridi et al.,2020).Neuronal activity during various brain states is primarily regulated by neurotransmitters(Schiemann et al.,2015),alongside non-synaptic mechanisms that operate on a slower timescale.The non-synaptic mechanisms are many,with the ionic composition of the extracellular space playing a significant role;altering extracellular ion concentrations affects sleep,arousal,electroencephalogram patterns,and behavioral states(Ding et al.,2016).

Psychiatric comorbidities in epilepsy:population co-occurrence,genetic correlations and causal effects

Background Psychiatric comorbidities are common in patients with epilepsy.Reasons for the co-occurrence of psychiatric conditions and epilepsy remain poorly understood.Aim We aimed to triangulate the relationship between epilepsy and psychiatric conditions to determine the extent and possible origins of these conditions.Methods Using nationwide Swedish health registries,we quantified the lifetime prevalence of psychiatric disorders in patients with epilepsy.We then used summarydata from genome-wide association studies to investigate whether the identified observational associations could be attributed to a shared underlying genetic aetiology using cross-trait linkage disequilibrium score regression.Finally,we assessed the potential bidirectional relationships using two-sample Mendelian randomisation.Results In a cohort of 7628495 individuals,we found that almost half of the 94435 individuals diagnosed with epilepsy were also diagnosed with a psychiatric condition in their lifetime(adjusted lifetime prevalence,44.09%;95%confidence interval(Cl)43.78%to 44.39%).We found evidence for a genetic correlation between epilepsy and some neurodevelopmental and psychiatric conditions.For example,we observed a genetic correlation between epilepsy and attention-deficit/hyperactivity disorder(r,=0.18,95%Cl 0.09 to 0.27,p<0.001)—a correlation that was more pronounced in focal epilepsy(r=0.23,95%CI 0.09 to 0.36,p<0.001).Findings from Mendelian randomisation using common genetic variants did not support bidirectional effects between epilepsy and neurodevelopmental or psychiatric conditions.Conclusions Psychiatric comorbidities are common in patients with epilepsy.Genetic correlations may partially explain some comorbidities;however,there is little evidence of a bidirectional relationship between the genetic liability of epilepsy and psychiatric conditions.These findings highlight the need to understand the role of environmental factors or rare genetic variations in the origins of psychiatric comorbidities in epilepsy.

Nrf2 as a potential target for the treatment of epilepsy

Epilepsy is a prevalent chronic brain disorder that is characterized by a persistent predisposition to recurrently generate epileptic seizures and is often associated with cognitive and psychological consequences.Epilepsy affects approximately 65 million individuals,including both males and females of all ages worldwide,and poses a significant burden on patients,their families,and the health system(Vezzani et al.,2019).