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CaMKII in global cerebral ischemia: mechanisms and therapeutic intervention
Organization UNIVERSITY OF COLORADO DENVERLocation Aurora, UNITED STATESPosted 15 Jan 2021Deadline 30 Nov 2025 โ ๏ธ
NIHUS FederalResearch GrantFY2025AD dementiaAblationAffectAlzheimer Type DementiaAlzheimer beta-ProteinAlzheimer disease dementiaAlzheimer sclerosisAlzheimer syndromeAlzheimer'sAlzheimer's Amyloid beta-ProteinAlzheimer's DiseaseAlzheimer's amyloidAlzheimers DementiaAmyloid Alzheimer's Dementia Amyloid ProteinAmyloid Beta-PeptideAmyloid Protein A4Amyloid beta-ProteinAmyloid ฮฒAmyloid ฮฒ-PeptideAmyloid ฮฒ-ProteinAsystoleAฮฒBNOSBindingBrainBrain Nervous SystemCaM KIICaM PK IICaM kinase IICaMKIICardiac ArrestCardiopulmonary ResuscitationCell Communication and SignalingCell DeathCell SignalingCell SurvivalCell ViabilityCerebral IschemiaClinical TrialsCognitionD-GlucoseDataDevelopmentDextroseDrug TherapyEncephalonExcitatory SynapseFamily suidaeFunctional impairmentFutureGeneticGlucoseHeart ArrestHumanHypothermiaImpairmentIndividualInformed ConsentInjectionsInterventionIntracellular Communication and SignalingIschemiaKO miceKinasesKnock-out MiceKnockout MiceLearningLiteratureLong-Term PotentiationMediatingMediatorMemoryMental DepressionMiceMice MammalsModelingModern ManMolecularMolecular InteractionMovementMurineMusMutant Strains MiceN-Methyl-D-Aspartate ReceptorsN-Methylaspartate ReceptorsNC-NOSNMDA Receptor-Ionophore ComplexNMDA ReceptorsNNOSNOS 1 proteinNOS type INOS1 proteinNerve CellsNerve UnitNeural CellNeural Constitutive Nitric Oxide SynthaseNeurocyteNeuronsNitric Oxide Synthase Type INull MouseO elementO2 elementOutcomeOxygenPathologicPathway interactionsPharmacological TreatmentPharmacotherapyPhosphatasesPhosphohydrolasesPhosphomonoesterasesPhosphoric Monoester HydrolasesPhosphorylationPhosphotransferase GenePhosphotransferasesPigsPreparationPrimary Senile Degenerative DementiaProtein PhosphorylationPublishingRegulationRisk FactorsRoleSignal TransductionSignal Transduction SystemsSignalingSuidaeSwineSynaptic plasticityTestingTherapeuticTherapeutic InterventionTimeTransphosphorylasesValidationVentricular FibrillationWorka beta peptideabetaamyloid betaamyloid-b proteinbeta amyloid fibrilbiological signal transductionbody movementbrain nitric oxide synthasecalcium-dependent CaM kinase IIcalmodulin-dependent protein kinase IIcardiac resuscitationclinical relevanceclinically relevantdepressiondeprivationdevelopmentaldrug interventiondrug treatmentexcitotoxicexcitotoxicityexperimentexperimental researchexperimental studyexperimentsheart resuscitationin vivoinhibitorintervention therapymotor impairmentmouse mutantmovement impairmentmovement limitationnNOS enzymenatural hypothermianecrocytosisnerve cell deathnerve cell lossneuron cell deathneuron cell lossneuron deathneuron lossneuronalneuronal NOSneuronal cell deathneuronal cell lossneuronal deathneuronal form of nitric oxide synthaseneuronal lossneuronal nitric oxide synthaseneuronal survivalneuroprotectionneuroprotectivenew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynitric oxide synthase 1novel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachoptimal therapiesoptimal treatmentspathwaypharmaceutical interventionpharmacological interventionpharmacological therapypharmacology interventionpharmacology treatmentpharmacotherapeuticsporcinepreparationspreventpreventingprimary degenerative dementiarestorationsenile dementia of the Alzheimer typesocial rolesoluble amyloid precursor proteinstandard of caresuidvalidations
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Project Summary/Abstract
The Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a central mediator of two opposing forms of NMDA-
receptor (NMDAR)-dependent synaptic plasticity: long-term potentiation (LTP) and depression (LTD).
Pathological overstimulation of NMDARs during cerebral ischemia causes excitotoxic neuronal cell death, and
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