Featured Publications
Convergent and Divergent Mechanisms of Epileptogenesis in mTORopathies
Nguyen LH, Bordey A. Convergent and Divergent Mechanisms of Epileptogenesis in mTORopathies. Frontiers In Neuroanatomy 2021, 15: 664695. PMID: 33897381, PMCID: PMC8064518, DOI: 10.3389/fnana.2021.664695.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsPI3K-mTOR pathwayCortical developmentGene variantsPotential therapeutic strategyIntractable epilepsyNeuronal placementTherapeutic strategiesAnimal modelsEpilepsyElectrophysiological phenotypeNeurodevelopmental disordersRapamycin complex 1Mechanistic targetEpileptogenesisIndependent mechanismsMTORopathiesGATOR1 complexPersonalized medicineDivergent mechanismsMosaic patternEverolimusMalformationsHyperactivityPathwayVariants
2022
Current Review in Basic Science: Animal Models of Focal Cortical Dysplasia and Epilepsy
Nguyen LH, Bordey A. Current Review in Basic Science: Animal Models of Focal Cortical Dysplasia and Epilepsy. Epilepsy Currents 2022, 22: 234-240. PMID: 36187145, PMCID: PMC9483763, DOI: 10.1177/15357597221098230.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsFocal cortical dysplasiaFCD type IIAnimal modelsCortical dysplasiaMechanisms of epileptogenesisNumerous animal modelsElectroclinical featuresIntractable epilepsyType IIFCD subtypesFrequent causeCortical developmentPrevalent causeNovel therapeuticsEpilepsyEarly lifeGene mutationsClinical applicationCurrent reviewDysplasiaTechnical considerationsMTORBasic scienceCause
2019
Hypervascularization in mTOR‐dependent focal and global cortical malformations displays differential rapamycin sensitivity
Zhang L, Huang T, Teaw S, Bordey A. Hypervascularization in mTOR‐dependent focal and global cortical malformations displays differential rapamycin sensitivity. Epilepsia 2019, 60: 1255-1265. PMID: 31125447, PMCID: PMC6558978, DOI: 10.1111/epi.15969.Peer-Reviewed Original ResearchConceptsBlood vesselsRapamycin treatmentVessel densityVessel abnormalitiesPostnatal day 14 miceAbsence of seizuresWild-type miceConditional transgenic miceTuberous sclerosis complexTypes of MCDDay 14 miceMCD modelFocal MCDMTOR blockersDysplastic neuronsFunctional outcomeEpilepsy treatmentSomatosensory cortexYoung miceFocal malformationsCortical developmentJuvenile miceTotal vessel lengthAnimal modelsTransgenic mice
2012
Understanding the Etiology of Tuberous Sclerosis Complex
Bordey A. Understanding the Etiology of Tuberous Sclerosis Complex. 2012 DOI: 10.21236/ada566455.Peer-Reviewed Original ResearchTuberous sclerosis complexTSC lesionsAnimal modelsDiscrete cortical lesionsGenetic multisystem disorderSevere neurological symptomsTsc1 inactivationCortical hyperexcitabilityNeurological symptomsCortical lesionsPerinatal lifeTSC patientsSeizure generationMultisystem disorderFormation of lesionsSignificant causeLesionsLesion formationEtiologyDisordersNovel technical approachHyperexcitabilityMorbidityPatientsSymptoms
2011
Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice
Feliciano DM, Su T, Lopez J, Platel JC, Bordey A. Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice. Journal Of Clinical Investigation 2011, 121: 1596-1607. PMID: 21403402, PMCID: PMC3069783, DOI: 10.1172/jci44909.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBase SequenceCell SizeCerebral CortexDisease Models, AnimalDNA PrimersFemaleGene Knockout TechniquesMiceMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMice, TransgenicPregnancySeizuresTOR Serine-Threonine KinasesTuberous SclerosisTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsConceptsTuberous sclerosis complexSeizure thresholdNeuronal populationsSigns of gliosisLower seizure thresholdContribution of astrocytesDiscrete neuronal populationsAutosomal dominant disorderHeterotopic nodulesCortical hyperexcitabilityCortical tubersCortical lesionsGlial reactivityIntractable seizuresCortical malformationsSoma sizeAnimal modelsTSC1 gene productAffected neuronsDendritic treeGiant cellsUtero electroporationMutant miceLesion formationMammalian target