2023
Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease
Datta D, Perone I, Morozov Y, Arellano J, Duque A, Rakic P, van Dyck C, Arnsten A. Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease. Cerebral Cortex 2023, 33: 11501-11516. PMID: 37874022, PMCID: PMC10724870, DOI: 10.1093/cercor/bhad382.Peer-Reviewed Original ResearchConceptsHCN1 channelsTau pathologyGlutamate synapsesEntorhinal cortexCalcium actionInternal calcium releaseEntorhinal cortex stellate cellsDorsolateral prefrontal cortexSusceptible neuronsInitial pathologySelective vulnerabilityEtiological factorsTau phosphorylationStellate cellsAlzheimer's diseaseSpecific neuronsCalcium releasePrefrontal cortexCortexSynapse strengthPathologyCalcium signalingCalbindinDiseaseNeuronsDeriving Schwann cells from hPSCs enables disease modeling and drug discovery for diabetic peripheral neuropathy
Majd H, Amin S, Ghazizadeh Z, Cesiulis A, Arroyo E, Lankford K, Majd A, Farahvashi S, Chemel A, Okoye M, Scantlen M, Tchieu J, Calder E, Le Rouzic V, Shibata B, Arab A, Goodarzi H, Pasternak G, Kocsis J, Chen S, Studer L, Fattahi F. Deriving Schwann cells from hPSCs enables disease modeling and drug discovery for diabetic peripheral neuropathy. Cell Stem Cell 2023, 30: 632-647.e10. PMID: 37146583, PMCID: PMC10249419, DOI: 10.1016/j.stem.2023.04.006.Peer-Reviewed Original ResearchConceptsDiabetic peripheral neuropathySchwann cellsPeripheral neuropathyPeripheral nervous systemPrimary Schwann cellsBupropion treatmentDiabetic patientsMyelin damageSensory dysfunctionPrimary gliaSelective vulnerabilityAntidepressant drugsHyperglycemic miceLower incidenceRetrospective analysisHuman pluripotent stem cellsSC deathNervous systemTherapeutic candidateHigh glucoseNeuropathyHealth recordsMolecular featuresStem cellsPluripotent stem cells
2019
Rationale for Targeting BCL6 in MLL-Rearranged B-ALL
Chan L, Hurtz C, Geng H, Ballabio E, Xiao G, Deb G, Khoury H, Armstrong S, Ernst P, Melnick A, Milne T, Müschen M. Rationale for Targeting BCL6 in MLL-Rearranged B-ALL. Blood 2019, 134: 1239. DOI: 10.1182/blood-2019-131565.Peer-Reviewed Original ResearchB-cell acute lymphoblastic leukemiaPharmacological inhibitionABT-199Group of patientsBCL6 expressionBone marrow biopsyPoor clinical outcomeAcute lymphoblastic leukemiaBCL2 inhibitor ABT-199BH3 mimetic ABT-199MLL gene rearrangementTransplant recipient miceMLL fusionsB-cell transformationClinical outcomesMarrow biopsyTreatment of MLLDismal outcomeLymphoblastic leukemiaRecipient miceNormal B cell developmentSelective vulnerabilityImmunohistochemical stainingInfant BSmall molecule inhibitors
2017
The distinct metabolic phenotype of lung squamous cell carcinoma defines selective vulnerability to glycolytic inhibition
Goodwin J, Neugent ML, Lee SY, Choe JH, Choi H, Jenkins DMR, Ruthenborg RJ, Robinson MW, Jeong JY, Wake M, Abe H, Takeda N, Endo H, Inoue M, Xuan Z, Yoo H, Chen M, Ahn JM, Minna JD, Helke KL, Singh PK, Shackelford DB, Kim JW. The distinct metabolic phenotype of lung squamous cell carcinoma defines selective vulnerability to glycolytic inhibition. Nature Communications 2017, 8: 15503. PMID: 28548087, PMCID: PMC5458561, DOI: 10.1038/ncomms15503.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAdultAgedAged, 80 and overAnimalsCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell Line, TumorCohort StudiesDeoxyglucoseFemaleFluorodeoxyglucose F18Gene Expression ProfilingGene Expression Regulation, NeoplasticGlucoseGlucose Transporter Type 1GlycolysisHumansHydroxybenzoatesLungLung NeoplasmsMaleMiceMice, NudeMiddle AgedPhenotypePositron-Emission TomographyPrognosisSurvival AnalysisUp-RegulationXenograft Model Antitumor AssaysConceptsNon-small cell lung cancerSquamous cell carcinomaLung SqCCCell carcinomaNSCLC subtypesGlycolytic inhibitionLung squamous cell carcinomaCell lung cancerPatient-derived xenograftsNSCLC tumor samplesNSCLC cell linesCancer Genome AtlasClinical presentationPoor prognosisTherapeutic optionsLung cancerPredominant subtypeDistinct metabolic phenotypesSelective vulnerabilityLung adenocarcinomaMurine modelTherapeutic strategiesSqCCTumor samplesMetabolic signatures
2014
cAMP-PKA phosphorylation of tau confers risk for degeneration in aging association cortex
Carlyle BC, Nairn AC, Wang M, Yang Y, Jin LE, Simen AA, Ramos BP, Bordner KA, Craft GE, Davies P, Pletikos M, Šestan N, Arnsten AF, Paspalas CD. cAMP-PKA phosphorylation of tau confers risk for degeneration in aging association cortex. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 5036-5041. PMID: 24707050, PMCID: PMC3977284, DOI: 10.1073/pnas.1322360111.Peer-Reviewed Original ResearchConceptsNeurofibrillary tanglesAssociation cortexAlzheimer's diseaseSpine apparatusPhosphorylated tauPattern of neurodegenerationLate-stage diseaseHigh-risk factorsNormal aged miceGenetic rodent modelsPrefrontal association cortexPrimary sensory cortexPrimary visual cortexAge-related increasePyramidal neuronsCorticocortical connectionsAged miceRisk factorsGlutamate synapsesSpine synapsesSelective vulnerabilityRodent modelsDendritic spinesSensory cortexProtein kinase phosphorylation
1988
Magnesium Inhibits Ischemia Induced Calcium Accumulation in Hilar Neurones: Possible Effect of Nmda-Receptor
Benveniste H, Diemer N. Magnesium Inhibits Ischemia Induced Calcium Accumulation in Hilar Neurones: Possible Effect of Nmda-Receptor. Advances In Behavioral Biology 1988, 35: 377-377. DOI: 10.1007/978-1-4684-5562-5_40.Peer-Reviewed Original ResearchHilar neuronsCA 1 pyramidal cellsN-methyl-D-aspartate receptorsCalcium accumulationIschemic brain damageExcessive calcium accumulationIschemic changesIschemic damageBrain damageNMDA receptorsPyramidal cellsSelective vulnerabilityHilar neuronesCalcium influxIrreversible morphological changesCalcium conductanceIschemiaMorphological damageExcessive accumulationNeuronsPivotal roleMorphological changesHoursPossible effectsDamage
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