2020
Pioglitazone activates paraoxonase-2 in the brain: A novel neuroprotective mechanism
Blackburn JK, Curry DW, Thomsen AN, Roth RH, Elsworth JD. Pioglitazone activates paraoxonase-2 in the brain: A novel neuroprotective mechanism. Experimental Neurology 2020, 327: 113234. PMID: 32044330, PMCID: PMC7089823, DOI: 10.1016/j.expneurol.2020.113234.Peer-Reviewed Original ResearchConceptsParaoxonase 2Novel neuroprotective mechanismParaoxonase-2 expressionAnti-diabetic drug pioglitazoneReactive oxygen species productionNeuroprotective strategiesNeuroprotective mechanismsBrain traumaMouse striatumOxygen species productionParkinson's diseaseAlzheimer's diseaseTherapeutic potentialPioglitazoneDiseaseOxidative stressDrug pioglitazoneSpecies productionBrainNeuroprotectionIschemiaStriatumExpressionPathologyTrauma
2018
Pre-implantation factor promotes neuroprotection by modulating long non-coding RNA H19 of the neuronal stem cells
Spinelli M, Ornaghi S, Schoeberlein A, Bordey A, Barnea E, Paidas M, Surbek D, Mueller M. Pre-implantation factor promotes neuroprotection by modulating long non-coding RNA H19 of the neuronal stem cells. Geburtshilfe Und Frauenheilkunde 2018, 78: 231-231. DOI: 10.1055/s-0038-1671458.Peer-Reviewed Original ResearchTAVI and the brain: update on definitions, evidence of neuroprotection and adjunctive pharmacotherapy.
Lansky A, Ghare MI, Tchétché D, Baumbach A. TAVI and the brain: update on definitions, evidence of neuroprotection and adjunctive pharmacotherapy. EuroIntervention 2018, 14: ab53-ab63. PMID: 30158096, DOI: 10.4244/eij-d-18-00454.Peer-Reviewed Original ResearchConceptsTranscatheter aortic valve implantationAortic stenosisAdjunctive pharmacotherapySevere symptomatic aortic stenosisIntermediate-risk patientsSymptomatic aortic stenosisHigh-risk patientsAortic valve implantationSurgical valve replacementEvidence of neuroprotectionNeurologic eventsDevastating complicationNeurologic injuryValve implantationValve replacementCurrent evidenceNeuroprotectionPharmacotherapyPatientsPreferred methodComplicationsStenosisInjuryStrokeIncidence
2017
Hippocampal insulin signaling and neuroprotection mediated by physical exercise in Alzheimer´s Disease
Kuga G, Botezelli J, Gaspar R, Gomes R, Pauli J, de Almeida Leme J. Hippocampal insulin signaling and neuroprotection mediated by physical exercise in Alzheimer´s Disease. Motriz Revista De Educação Física 2017, 23: e101608. DOI: 10.1590/s1980-6574201700si0008.Peer-Reviewed Original ResearchTreatment of ADAlzheimer's diseaseNeuronal survivalLow-grade inflammationAnti-inflammatory effectsNon-pharmacological alternativesAD genesisHippocampal insulinHippocampal neurodegenerationHippocampal neuroprotectionNeuroprotective mechanismsInsulin sensitivityEpidemiological studiesPhysical exerciseHippocampal integrityDiseaseInsulinNeuroprotectionExercisePreventionMolecular mechanismsSurvivalTreatmentIntense research effortsPowerful activatorΔN-Bcl-xL, a therapeutic target for neuroprotection
Park HA, Jonas EA. ΔN-Bcl-xL, a therapeutic target for neuroprotection. Neural Regeneration Research 2017, 12: 1791-1794. PMID: 29239317, PMCID: PMC5745825, DOI: 10.4103/1673-5374.219033.Peer-Reviewed Original ResearchΔN-BclNeuronal deathNeuronal viabilityMitochondrial dysfunctionPrimary hippocampal neuronsABT-737Excitotoxic injuryGlutamate toxicityHippocampal neuronsAnti-apoptotic proteinsTherapeutic targetB cellsPrimary neuronsNeuronal functionAcute productionNeuroprotectionAltered metabolismMitochondrial damageNeuronsCentral targetMitochondrial functionDysfunctionDeathMitochondrial anti-apoptotic proteinDependent effects
2016
Neurodegeneration and Neuroprotection in Glaucoma.
Gauthier AC, Liu J. Neurodegeneration and Neuroprotection in Glaucoma. The Yale Journal Of Biology And Medicine 2016, 89: 73-9. PMID: 27505018, PMCID: PMC4797839.Peer-Reviewed Original ResearchConceptsCentral nervous system degenerative disorderOptic nerve degenerationRetinal ganglion cellsLateral geniculate nucleusAdenosine receptor antagonistIntraocular pressureNerve degenerationNeurotrophic factorReceptor antagonistGanglion cellsGlaucoma progressionDisease progressionIrreversible blindnessGeniculate nucleusNew therapiesVisual cortexDegenerative disordersAxonal transportCell therapyGlaucomaOxidative stressTherapyDiseaseNeuroprotectionNeurodegeneration
2015
PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling
Mueller M, Schoeberlein A, Zhou J, Joerger-Messerli M, Oppliger B, Reinhart U, Bordey A, Surbek D, Barnea ER, Huang Y, Paidas M. PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling. Cell Death & Differentiation 2015, 22: 2078-2086. PMID: 25976303, PMCID: PMC4816111, DOI: 10.1038/cdd.2015.55.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsbcl-Associated Death ProteinBrain InjuriesCell Line, TumorCell SurvivalCyclic AMPCyclic AMP Response Element-Binding ProteinCyclic AMP-Dependent Protein KinasesDisease Models, AnimalGAP-43 ProteinMiceMicroRNAsNeuroprotective AgentsPeptidesProtein Kinase CProto-Oncogene Proteins c-bcl-2RatsRNA InterferenceSignal TransductionToll-Like Receptor 4ConceptsPreImplantation FactorCentral nervous system damageExperimental autoimmune encephalomyelitisPerinatal brain injuryBrain injury modelNervous system damageExpression of GAP43Autoimmune encephalomyelitisTLR4 expressionNeuronal lossPotential clinical applicationsCNS diseaseNeuronal deathBrain injuryClinical trialsInjury modelFast-track approvalProtective effectRodent modelsGAP-43NeuroprotectionSystem damageNeuronal growthProtein kinaseCortical architectureChapter 28 Mas and Neuroprotection in Stroke
Bennion D, Regenhardt R, Mecca A, Sumners C. Chapter 28 Mas and Neuroprotection in Stroke. 2015, 201-205. DOI: 10.1016/b978-0-12-801364-9.00028-6.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2012
Ucp2 Induced by Natural Birth Regulates Neuronal Differentiation of the Hippocampus and Related Adult Behavior
Simon-Areces J, Dietrich MO, Hermes G, Garcia-Segura LM, Arevalo MA, Horvath TL. Ucp2 Induced by Natural Birth Regulates Neuronal Differentiation of the Hippocampus and Related Adult Behavior. PLOS ONE 2012, 7: e42911. PMID: 22905184, PMCID: PMC3414493, DOI: 10.1371/journal.pone.0042911.Peer-Reviewed Original ResearchConceptsUCP2 expressionCellular stressHippocampal neuronsChemical inhibitionMitochondrial bioenergeticsNeuronal differentiationGenetic ablationNatural birthProtein 2Adult behaviorCell proliferationCritical roleAdult brainNeuronal numberExpressionBioenergeticsNeuronsBirthDifferentiationRegulationProliferationSynaptogenesisVitroNeuroprotectionHippocampus
2008
Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status
Waxman SG. Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status. Nature Reviews Neurology 2008, 4: 159-169. PMID: 18227822, DOI: 10.1038/ncpneuro0735.Peer-Reviewed Original ResearchChapter 22 α-Synuclein, CSPα, SNAREs and Neuroprotection in vivo
Chandra S, Südhof T. Chapter 22 α-Synuclein, CSPα, SNAREs and Neuroprotection in vivo. 2008, 295-308. DOI: 10.1016/b978-0-12-374028-1.00022-1.Peer-Reviewed Original ResearchΑ-synucleinDopamine replacement therapyMouse α-synucleinPathological functionsStriatal terminalsReplacement therapyPD treatmentNormal physiological functionSynaptic connectionsPresynaptic proteinsNeurodegenerative phenotypeΑ-deletionCysteine string proteinToxic gainAmino acid changesPhysiological functionsAcid changesNeuroprotectionPathogenesisTherapyFindingsNeurodegenerationNeuroprotection via nAChRs: the role of nAChRs in neurodegenerative disorders such as Alzheimer's and Parkinson's disease.
Picciotto MR, Zoli M. Neuroprotection via nAChRs: the role of nAChRs in neurodegenerative disorders such as Alzheimer's and Parkinson's disease. Frontiers In Bioscience-Landmark 2008, 13: 492-504. PMID: 17981563, DOI: 10.2741/2695.Peer-Reviewed Original ResearchConceptsAbility of nicotineNeurodegenerative disordersRole of nAChRsHuman neurodegenerationNeuroprotective agentsParkinson's diseaseDevelopmental stagesCellular effectsNicotine-mediated neuroprotectionRegimen of administrationDrug discoveryNicotine neuroprotectionNeuronal survivalNeuronal deathEpidemiological studiesNicotinic compoundsAlzheimer's diseaseRecent studiesNeuroprotectionDiseaseNicotineCompelling evidenceNAChRsVivoFull understanding
2007
Demyelinating diseases and potential repair strategies
Radtke C, Spies M, Sasaki M, Vogt PM, Kocsis JD. Demyelinating diseases and potential repair strategies. International Journal Of Developmental Neuroscience 2007, 25: 149-153. PMID: 17408905, PMCID: PMC2692731, DOI: 10.1016/j.ijdevneu.2007.02.002.Peer-Reviewed Original ResearchConceptsMultiple sclerosisInjury modelSpinal cord injuryCell-based strategiesAxon lossNerve compressionNeuroprotective potentialCord injuryFunctional outcomeClinical studiesMS lesionsTherapeutic goalsVulnerable axonsCellular transplantationNeurological disordersDemyelinationRemyelinationNeuroprotectionPotential repair strategiesCell typesSclerosisTransplantationInjuryLesionsAxonsNeuroinflammation and Excitotoxicity in Neurobiology of HIV-1 Infection and AIDS: Targets for Neuroprotection
Kaul M, Lipton S. Neuroinflammation and Excitotoxicity in Neurobiology of HIV-1 Infection and AIDS: Targets for Neuroprotection. 2007, 281-308. DOI: 10.1007/978-0-387-70830-0_13.Peer-Reviewed Original ResearchHuman immunodeficiency virus-1Central nervous systemMild behavioral abnormalitiesHIV-1 infectionImmune competent cellsImmunodeficiency virus-1Persistent health problemsFrank dementiaImmunodeficiency syndromeMotor dysfunctionInflammatory responseNeurological problemsParticular macrophagesBehavioral abnormalitiesNervous systemHealth problemsVirus 1InfectionBrainCell typesNeuroinflammationExcitotoxicityNeuroprotectionDysfunctionSyndrome
2006
Pharmacologic Neuroprotection in Patients with Spinal Cord Injury and the Efficacy of Early Decompressive Surgery
Poelstra K, Vaccaro A, Rao S, Patel A, Whang P, Kurd M, Stock G. Pharmacologic Neuroprotection in Patients with Spinal Cord Injury and the Efficacy of Early Decompressive Surgery. Topics In Spinal Cord Injury Rehabilitation 2006, 12: 63-76. DOI: 10.1310/c73a-3uac-8dff-h3vu.Peer-Reviewed Original ResearchRapid Hypoxia Preconditioning Protects Cortical Neurons From Glutamate Toxicity Through δ-Opioid Receptor
Zhang J, Qian H, Zhao P, Hong SS, Xia Y. Rapid Hypoxia Preconditioning Protects Cortical Neurons From Glutamate Toxicity Through δ-Opioid Receptor. Stroke 2006, 37: 1094-1099. PMID: 16514101, DOI: 10.1161/01.str.0000206444.29930.18.Peer-Reviewed Original ResearchConceptsDelta-opioid receptorsHypoxia preconditioningCortical neuronsNeuronal injuryGlutamate-induced neuronal injuryCultured rat cortical neuronsReceptor bindingSevere hypoxic injurySevere neuronal injuryRT-PCRCultured cortical neuronsMRNA levelsNMDA receptor expressionRat cortical neuronsΔ-opioid receptorsDOR mRNA levelsCulture day 8Short-term hypoxiaDOR mRNALactate dehydrogenase leakageHypoxic injuryGlutamate toxicityNeuronal viabilityReceptor expressionNeuroprotection
2005
Uncoupling protein 2 protects dopaminergic neurons from acute 1,2,3,6‐methyl‐phenyl‐tetrahydropyridine toxicity
Conti B, Sugama S, Lucero J, Winsky‐Sommerer R, Wirz SA, Maher P, Andrews Z, Barr AM, Morale MC, Paneda C, Pemberton J, Gaidarova S, Behrens MM, Beal F, Sanna PP, Horvath T, Bartfai T. Uncoupling protein 2 protects dopaminergic neurons from acute 1,2,3,6‐methyl‐phenyl‐tetrahydropyridine toxicity. Journal Of Neurochemistry 2005, 93: 493-501. PMID: 15816872, DOI: 10.1111/j.1471-4159.2005.03052.x.Peer-Reviewed Original ResearchConceptsDopaminergic neuronsParkinson's diseaseOxidative stressSpecific neuronal expressionTyrosine hydroxylase promoterTetrahydropyridine (MPTP) toxicityCatecholaminergic neuronsSubstantia nigraHydroxylase promoterLocomotor functionMouse modelNeuronal expressionAcute exposureTransgenic miceSporadic formsTwofold elevationUCP2 expressionDiseaseMarked reductionNeuronsMiceNeuroprotectionProtein 2UCP familyDrug targets
2003
Neuroprotection by Nicotine in Mouse Primary Cortical Cultures Involves Activation of Calcineurin and L-Type Calcium Channel Inactivation
Stevens TR, Krueger SR, Fitzsimonds RM, Picciotto MR. Neuroprotection by Nicotine in Mouse Primary Cortical Cultures Involves Activation of Calcineurin and L-Type Calcium Channel Inactivation. Journal Of Neuroscience 2003, 23: 10093-10099. PMID: 14602824, PMCID: PMC6740855, DOI: 10.1523/jneurosci.23-31-10093.2003.Peer-Reviewed Original ResearchMeSH Keywordsalpha7 Nicotinic Acetylcholine ReceptorAnimalsBungarotoxinsCalcineurinCalcineurin InhibitorsCalcium Channel BlockersCalcium Channels, L-TypeCells, CulturedCerebral CortexGlutamic AcidMiceMice, KnockoutNeuronsNeuroprotective AgentsNeurotoxinsNicotineNifedipineReceptors, NicotinicTacrolimusConceptsPrimary cortical culturesL-type channelsNicotine-mediated neuroprotectionCortical culturesNicotine pretreatmentIntracellular calciumCalcium influxActivation of calcineurinBeta2 subunitAlpha7-containing nAChRsL-type calcium channelsEffects of nicotineAbility of nicotineMouse primary cortical culturesNicotinic acetylcholine receptorsCalcium channel inactivationGlutamate excitotoxicityNeuroprotective effectsRole of calciumCalcineurin antagonistsCortical neuronsNeuronal excitabilityGlutamate applicationNeuroprotectionCalcium channels
1999
Attenuation of NMDA Receptor Activity and Neurotoxicity by Nitroxyl Anion, NO−
Kim W, Choi Y, Rayudu P, Das P, Asaad W, Arnelle D, Stamler J, Lipton S. Attenuation of NMDA Receptor Activity and Neurotoxicity by Nitroxyl Anion, NO−. Neuron 1999, 24: 461-469. PMID: 10571239, DOI: 10.1016/s0896-6273(00)80859-4.Peer-Reviewed Original Research
1998
Neuroprotective versus neurodestructive effects of NO‐related species
Lipton S, Choi Y, Sucher N, Chen H. Neuroprotective versus neurodestructive effects of NO‐related species. BioFactors 1998, 8: 33-40. PMID: 9699006, DOI: 10.1002/biof.5520080107.Peer-Reviewed Original ResearchConceptsNMDA receptorsCentral nervous systemNMDA receptor subunitsNeuronal injuryNeurodestructive effectsNervous systemRedox modulationReceptor subunitsNitric oxideExcessive Ca2Protective actionChannel activitySuperoxide anionNO groupReceptorsS-nitrosylationGroupDiverse tissuesNeuroprotectionInjuryBrain
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply