Search results for "epilepsy"

showing 10 items of 420 documents

A Recurrent De Novo PACS2 Heterozygous Missense Variant Causes Neonatal-Onset Developmental Epileptic Encephalopathy, Facial Dysmorphism, and Cerebel…

2018

International audience; Developmental and epileptic encephalopathies (DEEs) represent a large clinical and genetic heterogeneous group of neurodevelopmental diseases. The identification of pathogenic genetic variants in DEEs remains crucial for deciphering this complex group and for accurately caring for affected individuals (clinical diagnosis, genetic counseling, impacting medical, precision therapy, clinical trials, etc.). Whole-exome sequencing and intensive data sharing identified a recurrent de novo PACS2 heterozygous missense variant in 14 unrelated individuals. Their phenotype was characterized by epilepsy, global developmental delay with or without autism, common cerebellar dysgene…

Male0301 basic medicinePathologyPACS-2Vesicular Transport ProteinsPHENOTYPEBioinformaticsDISEASESensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Epilepsy0302 clinical medicineMissense mutationGlobal developmental delayAge of OnsetChildGenetics (clinical)Epileptic encephalopathyAPOPTOSIS3. Good healthcerebellar dysgenesisMutation Missense/geneticsintellectual disabilityChild PreschoolEpilepsy GeneralizedFemalePACS2CLINICAL EPILEPSYmedicine.medical_specialtyHeterozygoteGeneralized/geneticsPROTEINSGenetic counselingMutation MissenseMissense/geneticsNeonatal onsetBiologyDIAGNOSISVesicular Transport Proteins/geneticsFacial dysmorphism03 medical and health sciencesDysgenesisAll institutes and research themes of the Radboud University Medical CenterCerebellar DiseasesReportMENDELIAN DISORDERSGeneticsmedicineHumansGeneralized epilepsyPreschoolNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cerebellar Diseases/geneticsbusiness.industryMUTATIONSInfant NewbornCorrectionInfantFaciesNewbornmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationepilepsyAutismbusinessEpilepsy Generalized/genetics030217 neurology & neurosurgery
researchProduct

Pathology-selective antiepileptic effects in the focal freeze-lesion rat model of malformation of cortical development

2021

Malformations of cortical development (MCD) represent a group of rare diseases with severe clinical presentation as epileptic and pharmacoresistant encephalopathies. Morphological studies in tissue from MCD patients have revealed reduced GABAergic efficacy and increased intracellular chloride concentration in neuronal cells as important pathophysiological mechanisms in MCD. Also, in various animal models, alterations of GABAergic inhibition have been postulated as a predominant factor contributing to perilesional hyperexcitability. Along with this line, the NKCC1 inhibitor bumetanide has been postulated as a potential drug for treatment of epilepsy, mediating its antiepileptic effect by red…

Male0301 basic medicinePathologymedicine.medical_specialtyZonisamideInhibitory postsynaptic potentialCryosurgeryLesion03 medical and health sciencesEpilepsyOrgan Culture Techniques0302 clinical medicineSodium Potassium Chloride Symporter InhibitorsDevelopmental NeuroscienceSeizuresmedicineAnimals4-AminopyridineRats WistarBumetanideCerebral Cortexbusiness.industryCarbamazepinemedicine.diseaseRatsMicrogyrusMalformations of Cortical Development030104 developmental biologyNeurologyGABAergicAnticonvulsantsmedicine.symptombusiness030217 neurology & neurosurgeryBumetanidemedicine.drugExperimental Neurology
researchProduct

Comparative Study of the Effects Exerted by N-Valproyl-L-Phenylalanine and N-valproyl-L-tryptophan on CA1 Hippocampal Epileptiform Activity in Rat

2018

Background: The research on the improvement of epilepsy therapy is constantly growing. Valproyl-LPhenylalanine (VPA-Phen) and N-valproyl-L-tryptophan (VPA-Tryp) were synthesized to increase the antiepileptic efficacy of valproic acid. Methods: VPA-Phen and VPA-Tryp were comparatively tested on CA1 hippocampal epileptiform bursting activity obtained by increasing potassium and lowering calcium and magnesium concentrations in the fluid perfusing rat brain slices. Each slice was treated with a single concentration (0.2, 0.5, 1 mM) of VPA-Phen or VPA-Tryp. Both burst duration and interburst frequency, during and after treatment, were off-line compared with baseline values. For both parameters,…

Male0301 basic medicinePhenylalaninePotassiumchemistry.chemical_elementPharmacologyHippocampal formationCalciumInhibitory postsynaptic potentialHippocampusSettore BIO/09 - Fisiologia03 medical and health sciencesantiepileptic drug0302 clinical medicineDrug DiscoveryN-valproyl-L-tryptophanvalproic acid.medicineAnimalshippocampal epilepsyRats WistarPharmacologyValproic AcidEpilepsyValproyl-L-Phenylalanine (VPA-Phen)Dipeptidesinterictal burstRat brainAmino-acidic derivativeRats030104 developmental biologychemistryAnticonvulsantslipids (amino acids peptides and proteins)030217 neurology & neurosurgerymedicine.drugN-valproyl-L-phenylalanineCurrent Pharmaceutical Design
researchProduct

The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
researchProduct

A new family with an SLC9A6 mutation expanding the phenotypic spectrum of Christianson syndrome

2016

Using targeted next generation sequencing, we have identified a splicing mutation (c.526-9_526-5del) in the SLC9A6 gene in a 9-year-old boy with mild intellectual disability (ID), microcephaly, and social interaction disabilities. This intronic microdeletion leads to the skipping of exon 3 and to an in-frame deletion of 26 amino acids in the TM4 domain. It segregates with cognitive impairment or learning difficulties in other members of the family. Mutations in SLC9A6 have been reported in X-linked Christianson syndrome associating severe to profound intellectual deficiency and an Angelman-like phenotype with microcephaly, absent speech, ataxia with progressive cerebellar atrophy, ophthalmo…

Male0301 basic medicineProbandMicrocephalyDNA Mutational Analysisx-chromosome inactivationSLC9A6Gene mutationexchangerEpilepsyOcular Motility Disorders0302 clinical medicineangelman-syndromeX Chromosome InactivationIntellectual disabilitymicrocephalyChild10. No inequalityGenetics (clinical)Sequence DeletionGeneticsBrainGenetic Diseases X-LinkedtoolMagnetic Resonance ImagingPedigree3. Good healthPhenotypeFemaleCerebellar atrophyChristianson syndromemedicine.symptomAdultHeterozygoteSodium-Hydrogen ExchangersAtaxiaAdolescentlearning disabilities linked mental-retardation03 medical and health sciencescerebellar atrophyIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyAngelman syndromeGeneticsmedicineHumansFamilygeneGenetic Association Studiesbusiness.industryFaciesmedicine.disease030104 developmental biologysplicing signalsMutationepilepsyAtaxiaRNA Splice Sitesbusiness030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

Generation of an iPSC line (UNINAi001-A) from a girl with neonatal-onset epilepsy and non-syndromic intellectual disability carrying the homozygous K…

2021

Abstract Heterozygous variants in the KCNQ3 gene cause epileptic and/or developmental disorders of varying severity. Here we describe the generation of induced pluripotent stem cells (iPSCs) from a 9-year-old girl with pharmacodependent neonatal-onset epilepsy and intellectual disability who carry a homozygous single-base duplication in exon 12 of KCNQ3 (NM_004519.3: KCNQ3 c.1599dup; KCNQ3 p.PHE534ILEfs*15), and from a non-carrier brother of the proband. For iPSC generation, non-integrating episomal plasmid vectors were used to transfect fibroblasts isolated from skin biopsies. The obtained iPSC lines had a normal karyotype, showed embryonic stem cell-like morphology, expressed pluripotency…

Male0301 basic medicineProbandQH301-705.5Induced Pluripotent Stem CellsBiology03 medical and health sciencesEpilepsyExon0302 clinical medicineIntellectual DisabilityGene duplicationIntellectual disabilitymedicineHumansBiology (General)ChildInduced pluripotent stem cellEpilepsySiblingsHomozygoteCell DifferentiationKaryotypeCell BiologyGeneral Medicinemedicine.diseaseEmbryonic stem cell030104 developmental biologyCancer researchFemale030217 neurology & neurosurgeryDevelopmental Biology
researchProduct

The FAAH inhibitor URB597 suppresses hippocampal maximal dentate afterdischarges and restores seizure-induced impairment of short and long-term synap…

2017

Synthetic cannabinoids and phytocannabinoids have been shown to suppress seizures both in humans and experimental models of epilepsy. However, they generally have a detrimental effect on memory and memory-related processes. Here we compared the effect of the inhibition of the endocannabinoid (eCB) degradation versus synthetic CB agonist on limbic seizures induced by maximal dentate activation (MDA) acute kindling. Moreover, we investigated the dentate gyrus (DG) granule cell reactivity and synaptic plasticity in naïve and in MDA-kindled anaesthetised rats. We found that both the fatty acid amide hydrolase (FAAH) inhibitor URB597 and the synthetic cannabinoid agonist WIN55,212-2 displayed AM…

Male0301 basic medicinemedicine.medical_treatmentLong-Term Potentiationlcsh:MedicineBrain -- Diseases -- DiagnosisSynaptic TransmissionEpilepsy -- Alternative treatmentchemistry.chemical_compoundEpilepsy0302 clinical medicineFatty acid amide hydrolaselcsh:ScienceTemporal lobe epilepsyInhibitionNeuronal PlasticityMultidisciplinaryLong-term potentiationmedicine.anatomical_structureAnesthesiaBenzamidesHippocampus (Brain)medicine.medical_specialtyArticleAmidohydrolases03 medical and health sciencesSeizuresInternal medicinemedicineAnimalsAuthor CorrectionEpilepsyCannabinoidsDentate gyruslcsh:RURB597medicine.diseaseGranule cellHippocampus (Brain) -- PhysiologyRats030104 developmental biologyEndocrinologychemistryDentate GyrusSynaptic plasticitylcsh:QNeuroplasticityCarbamatesCannabinoid030217 neurology & neurosurgery
researchProduct

Lamotrigine differently modulates 7-Nitroindazole and L-Arginine influence on Rat Maximal Dentate Gyrus Activation

2007

The effects induced on the maximal dentate gyrus activation (MDA) by administering the anticonvulsant lamotrigine (LTG), the selective inhibitor of neuronal nitric oxide synthase 7-nitroindazole (7-NI) and the precursor of nitric oxide (NO) synthesis L-arginine, alone or in combination, were studied in urethane anaesthetized rats. Either 7-NI or LTG alone administration reduced the number of convulsing animals following angular bundle (AB) stimulation; their combined treatment induced a further increase of the anticonvulsant effect as also demonstrated by the decrease of MDA and afterdischarge (AD) durations in the animals still responding to AB stimulation. On the contrary, the injection o…

Male7-NitroindazoleIndazolesArgininemedicine.medical_treatmentStimulationPharmacologyLamotrigineArginineLamotrigineNitric OxideSettore BIO/09 - FisiologiaNitric oxidechemistry.chemical_compoundSeizuresmedicineAnimalsEnzyme InhibitorsRats WistarBiological PsychiatryTriazinesDentate gyrusElectric StimulationRatsPsychiatry and Mental healthAnticonvulsantNeurologychemistryDentate GyrusAnticonvulsantsNeurology (clinical)Neuronal Nitric Oxide Synthasemedicine.drugLAMOTRIGINE NITRIC OXIDE EPILEPSY CONTROL
researchProduct

In the rat maximal dentate activation model of partial complex epilepsy, the anticonvulsant activity of levetiracetam is modulated by nitric oxide-ac…

2009

The effects of nitric oxide-active drugs on the anticonvulsant action of the antiepileptic drug levetiracetam in an experimental model of partial complex seizures named maximal dentate gyrus activation were studied in rats. Levetiracetam was given alone or in combination with 7-nitroindazole, a preferential inhibitor of neuronal nitric oxide synthase, or with L: -arginine, the precursor of nitric oxide synthesis. The maximal dentate activation parameters were the time of latency and the durations of maximal dentate activation and afterdischarge responses. The administration of levetiracetam showed an anticonvulsant effect that was increased when given in combination with 7-nitroindazole. Th…

Male7-NitroindazoleIndazolesLevetiracetamMaximal dentate activation - Nitric oxide - Levetiracetam - Modulation - 7-Nitroindazolemedicine.medical_treatmentNitric Oxide Synthase Type IPharmacologyArginineNitric OxideSettore BIO/09 - FisiologiaNitric oxideEpilepsychemistry.chemical_compoundEpilepsy Complex PartialmedicineAnimalsDrug InteractionsEnzyme InhibitorsRats WistarMaximal dentate activation Nitric oxide Levetiracetam Modulation 7-NitroindazoleBiological PsychiatryDose-Response Relationship DrugChemistryDentate gyrusPiracetammedicine.diseaseEffective dose (pharmacology)PiracetamRatsPsychiatry and Mental healthDisease Models AnimalDrug CombinationsAnticonvulsantNeurologyDentate GyrusAnticonvulsantsNeurology (clinical)Levetiracetammedicine.drugJournal of neural transmission (Vienna, Austria : 1996)
researchProduct

High dose of 8-OH-DPAT decreases maximal dentate gyrus activation and facilitates granular cell plasticity in vivo.

2013

Although several studies have emphasized a crucial role for the serotonergic system in the control of hippocampal excitability, the role of serotonin (5-HT) and its receptors in normal and pathologic conditions, such as temporal lobe epilepsy (TLE), is still unclear. The present study was therefore designed firstly to investigate the acute effect of 8-OH-DPAT, a mixed 5-HT1A/7 receptor agonist, at a high dose (1 mg/kg, i.p.) known to have antiepileptic properties, in a model of acute partial epilepsy in rats. For this purpose, a maximal dentate activation (MDA) protocol was used to measure electrographic seizure onset and duration. In addition, the effect of 8-OH-DPAT on in vivo dentate gyr…

MaleAgonistSerotoninmedicine.medical_specialtymedicine.drug_classSerotonergic1AHippocampal formationDentate gyruSerotonergicSettore BIO/09 - FisiologiaRats Sprague-Dawleychemistry.chemical_compoundEpilepsyMemoryInternal medicineAnimalsMedicineDentate gyrusTemporal lobe epilepsySerotonin receptor5-HT receptor8-Hydroxy-2-(di-n-propylamino)tetralinNeuronal PlasticityDepressionbusiness.industry8-OH-DPATGeneral NeuroscienceDentate gyrusLong-term potentiationmedicine.diseaseRatsSerotonin Receptor AgonistsEndocrinologyDepression Mentalnervous systemchemistryReceptors SerotoninDentate Gyrusbusinessdrugs.Neuroscience
researchProduct