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
2020
Mitochondrial Dysfunction and Ovarian Aging
Kasapoğlu I, Seli E. Mitochondrial Dysfunction and Ovarian Aging. Endocrinology 2020, 161: bqaa001. PMID: 31927571, DOI: 10.1210/endocr/bqaa001.Peer-Reviewed Original Research
2019
Deletion of the creatine transporter gene in neonatal, but not adult, mice leads to cognitive deficits
Udobi KC, Delcimmuto N, Kokenge AN, Abdulla ZI, Perna MK, Skelton MR. Deletion of the creatine transporter gene in neonatal, but not adult, mice leads to cognitive deficits. Journal Of Inherited Metabolic Disease 2019, 42: 966-974. PMID: 31209903, PMCID: PMC6739135, DOI: 10.1002/jimd.12137.Peer-Reviewed Original ResearchConceptsMorris water mazeKnockout miceSLC6A8 geneWater mazeBrain developmentCrT deficiencyTamoxifen-inducible Cre recombinaseAdministration of tamoxifenNovel object recognitionCreatine transporter geneProper control groupSevere intellectual disabilityBrain CrControl miceAdenosine triphosphateHuman ubiquitin C promoterAdult miceBehavioral testingControl groupPrevalent causeLocomotor activityUbiquitin C promoterCognitive deficitsMiceCre recombinase
2013
Amyloid-β induced signaling by cellular prion protein and Fyn kinase in Alzheimer disease
Um JW, Strittmatter SM. Amyloid-β induced signaling by cellular prion protein and Fyn kinase in Alzheimer disease. Prion 2013, 7: 37-41. PMID: 22987042, PMCID: PMC3609048, DOI: 10.4161/pri.22212.Peer-Reviewed Original ResearchConceptsCellular prion proteinPrion proteinSignal transduction downstreamTransduction downstreamAlzheimer's diseaseFyn kinaseFunctional consequencesAβ oligomersAmyloid-β OligomersNeuronal surfaceHigh-affinity receptorOligomer complexesAD-related phenotypesCentral roleProteinAD pathogenesisRecent evidencePrevalent causeTherapeutic interventionsFynKinaseOligomersPhenotypeDiseaseDownstreamChapter 66 Disorders of Calcium Metabolism
Dumitru C, Wysolmerski J. Chapter 66 Disorders of Calcium Metabolism. 2013, 2273-2309. DOI: 10.1016/b978-0-12-381462-3.00066-5.Peer-Reviewed Original ResearchCalcium metabolismCalcium levelsParathyroid hormone-related proteinMulti-organ dysfunctionHormone-related proteinMetabolic bone disordersExtracellular calcium levelsParathyroid hormone receptorPrinciples of managementParathyroid hormoneBone metabolismBone disordersPrevalent causeCalcium homeostasisOrgan systemsHormone receptorsDisease statesHypercalcemiaHypocalcemiaDisordersNormal regulationHormoneMetabolismReceptorsCritical role
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