Search results for "zur"

showing 10 items of 321 documents

Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures.

2020

The Alzheimer disease-associated multifunctional low-density lipoprotein receptor-related protein-1 is expressed in the brain. Recent studies uncovered a role of this receptor for the appropriate functioning of neural stem cells, oligodendrocytes, and neurons. The constitutive knock-out (KO) of the receptor is embryonically lethal. To unravel the receptors' role in the developing brain we generated a mouse mutant by specifically targeting radial glia stem cells of the dorsal telencephalon. The low-density lipoprotein receptor-related protein-1 lineage-restricted KO female and male mice, in contrast to available models, developed a severe neurological phenotype with generalized seizures duri…

0301 basic medicineMaleEpendymoglial CellsBiology03 medical and health sciencesCellular and Molecular NeuroscienceEpilepsyMice0302 clinical medicineProsencephalonSeizuresmedicineAnimalsReceptors LipoproteinLipoprotein receptor-related proteinmedicine.diseaseNeural stem cellLipoproteins LDL030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTissue Plasminogen ActivatorForebrainFemaleSynaptic signalingStem cellPostsynaptic densityNeuroscience030217 neurology & neurosurgeryAstrocyteGliaREFERENCES
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IQSEC2-related encephalopathy in males and females: a comparative study including 37 novel patients.

2019

Variants in IQSEC2, escaping X inactivation, cause X-linked intellectual disability with frequent epilepsy in males and females. We aimed to investigate sex-specific differences.

0301 basic medicineMaleGénétique clinique[SDV]Life Sciences [q-bio]MedizinPhysiology030105 genetics & hereditySeizures/epidemiologyEpilepsyBrain Diseases/epidemiologyX-linked inheritanceIntellectual disabilityGuanine Nucleotide Exchange FactorsProtein IsoformsMissense mutationGenetics(clinical)10. No inequalityNon-U.S. Gov'tGenetics (clinical)X-linked recessive inheritanceComputingMilieux_MISCELLANEOUSBrain DiseasesSex CharacteristicsResearch Support Non-U.S. Gov'tBrainSciences bio-médicales et agricoles3. Good healthPedigreePhenotypeintellectual disabilityFemaleBrain/growth & developmentSex characteristicsGénétique moléculaireGuanine Nucleotide Exchange Factors/geneticsEncephalopathyResearch SupportX-inactivationArticle03 medical and health sciencesSeizuresProtein Isoforms/geneticsmedicineJournal ArticleIQSEC2HumansIntellectual Disability/epidemiology[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfant NewbornisoformsCorrectionInfantmedicine.diseaseNewbornHuman genetics030104 developmental biologyMutationepilepsyHuman medicinebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Heterozygous Variants in KDM4B Lead to Global Developmental Delay and Neuroanatomical Defects

2020

International audience; KDM4B is a lysine-specific demethylase with a preferential activity on H3K9 tri/di-methylation (H3K9me3/2)-modified histones. H3K9 tri/di-demethylation is an important epigenetic mechanism responsible for silencing of gene expression in animal development and cancer. However, the role of KDM4B on human development is still poorly characterized. Through international data sharing, we gathered a cohort of nine individuals with mono-allelic de novo or inherited variants in KDM4B. All individuals presented with dysmorphic features and global developmental delay (GDD) with language and motor skills most affected. Three individuals had a history of seizures, and four had a…

0301 basic medicineMaleJumonji Domain-Containing Histone Demethylases[SDV]Life Sciences [q-bio]Developmental DisabilitiesCorpus callosumHippocampusEpigenesis GeneticHistonesMice0302 clinical medicineNeurodevelopmental disorderPolymicrogyriaGlobal developmental delayAgenesis of the corpus callosumGenetics (clinical)BrainMagnetic Resonance Imaging[SDV] Life Sciences [q-bio]intellectual disabilityBrain sizeFemaledysmorphic hippocampiSignal TransductionHeterozygoteheterozygous variantglobal developmental delayBiologyNervous System MalformationsMethylation03 medical and health sciencesSeizuresReportKDM4BGeneticsmedicineAnimalsHumansneurodevelopmental disorder.Dentate gyrusGenetic VariationJMJD2Bmedicine.diseaseneurodevelopmental disorder030104 developmental biologyagenesis of the corpus callosumNeuroscienceProtein Processing Post-Translational030217 neurology & neurosurgeryVentriculomegalyAmerican journal of human genetics
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Targeting brain and peripheral plasticity of the lipidome in acute kainic acid-induced epileptic seizures in mice via quantitative mass spectrometry.

2017

Epilepsy is a highly common chronic neurological disorder, manifested in many different types, affecting ~1% of the worldwide human population. The molecular mechanisms of epileptogenesis have not yet been clarified, and pharmacoresistance exhibited by 30-40% of epilepsy patients remains a major obstacle in medical care. Growing evidence indicates a role of lipid signalling pathways in epileptogenesis, thus lipid signals emerge as potential biomarkers for the onset and evolving course of the epileptic disorder, as well as potential therapeutic agents and targets. For this purpose, we applied a lipidomic strategy to unravel lipid alterations in brain regions, periphery tissues and plasma tha…

0301 basic medicineMaleKainic acidPopulationPharmacologyBiologyEpileptogenesisMass Spectrometry03 medical and health sciencesEpilepsychemistry.chemical_compoundOleoylethanolamideMice0302 clinical medicinemedicineAnimalseducationMolecular BiologyLungPalmitoylethanolamideeducation.field_of_studyEpilepsyKainic AcidNeuronal PlasticityFatty AcidsBrainHeartCell BiologyAnandamidemedicine.diseaseLipidsMice Inbred C57BL030104 developmental biologychemistrylipids (amino acids peptides and proteins)Epileptic seizuremedicine.symptom030217 neurology & neurosurgerySignal TransductionBiochimica et biophysica acta. Molecular and cell biology of lipids
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Autosomal-Recessive Mutations in AP3B2, Adaptor-Related Protein Complex 3 Beta 2 Subunit, Cause an Early-Onset Epileptic Encephalopathy with Optic At…

2016

International audience; Early-onset epileptic encephalopathy (EOEE) represents a heterogeneous group of severe disorders characterized by seizures, interictal epileptiform activity with a disorganized electroencephalography background, developmental regression or retardation, and onset before 1 year of age. Among a cohort of 57 individuals with epileptic encephalopathy, we ascertained two unrelated affected individuals with EOEE associated with developmental impairment and autosomal-recessive variants in AP3B2 by means of whole-exome sequencing. The targeted sequencing of AP3B2 in 86 unrelated individuals with EOEE led to the identification of an additional family. We gathered five addition…

0301 basic medicineMaleMicrocephalyDevelopmental DisabilitiesPostnatal microcephalycopper-metabolismEpilepsy0302 clinical medicineexpansionhermansky-pudlak-syndromeddc:576.5Age of OnsetChilddisordersGenetics (clinical)seizuresGeneticsMEDNIK syndromeSyndrome3. Good healthPedigreeintellectual disabilityChild Preschoolmednik syndromeMicrocephalyFemaleDevelopmental regressionAdaptor Protein Complex 3Genes RecessiveBiologyAP3B103 medical and health sciencesAtrophyReport[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansAdaptor Protein Complex beta SubunitsmousediseaseEpilepsyap-4 deficiencyInfant NewbornInfantmedicine.diseaseOptic Atrophy030104 developmental biologyMutationHermansky–Pudlak syndrome030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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PRRT2 gene variant in a child with dysmorphic features, congenital microcephaly, and severe epileptic seizures: genotype-phenotype correlation?

2019

Abstract Background Mutations in Proline-rich Transmembrane Protein 2 (PRRT2) have been primarily associated with individuals presenting with infantile epilepsy, including benign familial infantile epilepsy, benign infantile epilepsy, and benign myoclonus of early infancy, and/or with dyskinetic paroxysms such as paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, and exercise-induced dyskinesia. However, the clinical manifestations of this disorder vary widely. PRRT2 encodes a protein expressed in the central nervous system that is mainly localized in the pre-synaptic neurons and is involved in the modulation of synaptic neurotransmitter release. The anomalous functio…

0301 basic medicineMaleMicrocephalyMutation MissenseCase ReportNerve Tissue ProteinsBioinformaticsRisk AssessmentSeverity of Illness Index03 medical and health sciences0302 clinical medicineRare DiseasesSeizuresmedicineHumansGenetic Predisposition to DiseaseGenetic TestingExome sequencingGenetic Association StudiesBenign familial infantile epilepsyDysmorphic featuresbusiness.industryEpileptic encephalopathylcsh:RJ1-570InfantMembrane Proteinslcsh:PediatricsParoxysmal dyskinesiamedicine.diseaseBody Dysmorphic DisordersPrognosisPRRT2 mutationMagnetic Resonance Imaging030104 developmental biologyDyskinesiaMicrocephalymedicine.symptomPRRT2 mutation Dysmorphic features Microcephaly Epileptic encephalopathybusinessMyoclonus030217 neurology & neurosurgeryPRRT2Benign infantile epilepsy
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Intravenous thrombolysis for suspected ischemic stroke with seizure at onset

2019

Objective Seizure at onset (SaO) has been considered a relative contraindication for intravenous thrombolysis (IVT) in patients with acute ischemic stroke, although this appraisal is not evidence based. Here, we investigated the prognostic significance of SaO in patients treated with IVT for suspected ischemic stroke. Methods In this multicenter, IVT-registry-based study we assessed the association between SaO and symptomatic intracranial hemorrhage (sICH, European Cooperative Acute Stroke Study II definition), 3-month mortality, and 3-month functional outcome on the modified Rankin Scale (mRS) using unadjusted and adjusted logistic regression, coarsened exact matching, and inverse probabil…

0301 basic medicineMalemedicine.medical_specialtymedicine.medical_treatmentLogistic regressionGUIDELINESCLASSIFICATION3124 Neurology and psychiatryBrain IschemiaEARLY MANAGEMENT03 medical and health sciences0302 clinical medicineALTEPLASEModified Rankin ScaleSeizuresMIMICSInternal medicineMedicineHumansThrombolytic TherapyPLASMINOGEN-ACTIVATOR610 Medicine & healthStrokeContraindicationPOPULATIONAgedAged 80 and overHEALTH-CARE PROFESSIONALSbusiness.industryConfounding3112 NeurosciencesOdds ratioThrombolysisASSOCIATIONMiddle Agedmedicine.diseasePrognosisConfidence intervalStroke030104 developmental biologyTreatment OutcomeNeurologySAFETYFemaleNeurology (clinical)business030217 neurology & neurosurgery
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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EAST/SeSAME syndrome: Review of the literature and introduction of four new Latvian patients.

2018

EAST (Epilepsy, Ataxia, Sensorineural deafness, Tubulopathy) or SeSAME (Seizures, Sensorineural deafness, Ataxia, Mental retardation, and Electrolyte imbalance) syndrome is a rare autosomal recessive syndrome first described in 2009 independently by Bockenhauer and Scholl. It is caused by mutations in KCNJ10, which encodes Kir4.1, an inwardly rectifying K+ channel found in the brain, inner ear, kidney and eye. To date, 16 mutations and at least 28 patients have been reported. In this paper, we review mutations causing EAST/SeSAME syndrome, clinical manifestations in detail, and efficacy of treatment in previously reported patients. We also report a new Latvian kindred with 4 patients. In co…

0301 basic medicinePediatricsmedicine.medical_specialtyAtaxiaHearing Loss SensorineuralKCNJ10030105 genetics & hereditySensorineural deafnessKidney03 medical and health sciencesEpilepsyTubulopathySeizuresIntellectual DisabilityIntellectual disabilityGeneticsmedicineEAST syndromeHumansEye AbnormalitiesPotassium Channels Inwardly RectifyingGenetics (clinical)SeSAME syndromebiologybusiness.industryBrainmedicine.diseaseLatvia030104 developmental biologyPhenotypeEar InnerMutationbiology.proteinmedicine.symptombusinessClinical genetics
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