2012
Myelin, Impulse Conduction, and the Pathophysiology of Demyelination
Bangalore L, Waxman S. Myelin, Impulse Conduction, and the Pathophysiology of Demyelination. 2012, 529-542. DOI: 10.1093/med/9780199794591.003.0042.Peer-Reviewed Original ResearchPathophysiology of demyelinationNormal brain functionMultiple sclerosisGlial cellsParkinson's diseaseNeurological diseasesAlzheimer's diseasePsychiatric conditionsImpulse conductionBrain functionDiseaseGliaNeuronsBasic biologyCell anatomyConcerted actionCellsDemyelinationSclerosisPathophysiologyStrokeCentral roleBrainMyelinAxonal Protection with Sodium Channel Blocking Agents in Models of Multiple Sclerosis
Black J, Smith K, Waxman S. Axonal Protection with Sodium Channel Blocking Agents in Models of Multiple Sclerosis. 2012, 179-201. DOI: 10.1007/978-1-4614-2218-1_8.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisMultiple sclerosisSodium channelsAspects of MSAcute MS plaquesChronic inactive plaquesSignificant axonal damageImmune cell infiltrationSodium channel blockadeChannel Blocking AgentsSpinal cord axonsWhite matter axonsVoltage-gated sodium channelsAction potential conductionInactive plaquesClinical disabilityAutoimmune encephalomyelitisAxonal protectionNeuroinflammatory disordersNeurological deficitsNeuroprotective therapiesAxonal damageIschemia injuryAxonal degenerationAxonal injury
2010
Sodium channel expression and function in multiple sclerosis
Bangalore L, Black J, Carrithers M, Waxman S. Sodium channel expression and function in multiple sclerosis. 2010, 29-43. DOI: 10.1017/cbo9780511781698.005.Peer-Reviewed Original ResearchMultiple sclerosisRecovery of functionSodium channel expressionHealth care advisorsMechanisms of recoveryNeurorehabilitation programChannel expressionSpecific syndromesTherapeutic interventionsCare advisorsClinical rehabilitationEfficient therapySclerosisDisease mechanismsPatientsCliniciansNeurorehabilitationInterventionBasic scienceSocial participationPathophysiologySyndromeTherapyNeuroplasticity
2009
Multiple Sclerosis
Preiningerova J, Bomprezzi R, Vollmer T, Waxman S. Multiple Sclerosis. 2009 DOI: 10.1002/9780470015902.a0000192.pub2.Peer-Reviewed Original ResearchCentral nervous systemMagnetic resonance imagingMultiple sclerosisImmune attackMS patientsNeurological disabilityInflammatory diseasesT cellsNervous systemTreatment of MSPathogenesis of MSProgression of MSBrain magnetic resonance imagingYoung womenAutoaggressive T cellsRegulatory T cellsLong-term disabilityDiseases of myelinMajor advancesDisease activityOngoing inflammationImmunotherapeutic strategiesAutoimmune diseasesClinical appearanceHumoral mechanisms
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 Research
2006
Axonal conduction and injury in multiple sclerosis: the role of sodium channels
Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Reviews Neuroscience 2006, 7: 932-941. PMID: 17115075, DOI: 10.1038/nrn2023.Peer-Reviewed Original ResearchConceptsAxonal degenerationSodium channelsChannel isoformsDistinct pathophysiological rolesKey PointsMultiple sclerosisMultiple neurological deficitsRelapsing-remitting courseRestoration of conductionDegeneration of axonsCerebellar Purkinje neuronsVoltage-gated sodium channelsContext of demyelinationNeurological deficitsProgressive courseMultiple sclerosisAxonal conductionDisease progressionNav1.8 channelsConduction failurePathophysiological rolePurkinje neuronsCNS axonsFiring patternsLoss of coordinationAberrant expressionTranscriptional Channelopathies of the Nervous System
Waxman S. Transcriptional Channelopathies of the Nervous System. 2006 DOI: 10.1002/9780470015902.a0006086.Peer-Reviewed Original ResearchSodium channel geneChannel genesTranscriptional channelopathiesSodium channel gene expressionChannel gene expressionGene expressionPeripheral nerve injurySpinal sensory neuronsGenesDysregulated expressionNerve injuryMultiple sclerosisSensory neuronsNervous systemCerebellar functionRecent studiesExpressionChannelopathiesAbstract Recent studiesHyperexcitabilitySclerosisInjuryNeuronsCells
2005
Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions
Frohman E, Filippi M, Stuve O, Waxman S, Corboy J, Phillips J, Lucchinetti C, Wilken J, Karandikar N, Hemmer B, Monson N, De Keyser J, Hartung H, Steinman L, Oksenberg J, Cree B, Hauser S, Racke M. Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions. JAMA Neurology 2005, 62: 1345-1356. PMID: 16157741, DOI: 10.1001/archneur.62.9.1345.Peer-Reviewed Original ResearchConceptsMultiple sclerosisProgression of MSCause of progressionMechanisms of progressionMS exacerbationDisease courseInflammatory cascadeClinical manifestationsTherapeutic strategiesDisease processTreatment interventionsEvidence-based observationsEmergence of disabilityProgressionDiseasePotential mechanismsTreatment effectsSclerosisProgressive stagesNovel research initiativesExacerbationTherapyIllnessMajor advancementsExpert perspectives22 Neuronal Blocking Factors in Demyelinating Diseases
Cummins T, Waxman S. 22 Neuronal Blocking Factors in Demyelinating Diseases. 2005, 317-326. DOI: 10.1016/b978-012738761-1/50023-7.Peer-Reviewed Original ResearchVoltage-gated sodium channelsGuillain-Barré syndromeMultiple sclerosisSodium channelsChronic inflammatory demyelinating polyneuropathyInflammatory demyelinating polyneuropathyInflammatory demyelinating diseaseBlocking factorsDemyelinating polyneuropathyDemyelinating diseaseClinical deficitsAxonal degenerationInflammatory diseasesConduction blockSodium currentNitric oxideExperimental modelDiseaseImpulse transmissionSclerosisBiological toxinsDemyelinationFactorsPolyneuropathyCytokines29 Blocking the Axonal Injury Cascade Neuroprotection in Multiple Sclerosis and Its Models
Waxman S, Lo A. 29 Blocking the Axonal Injury Cascade Neuroprotection in Multiple Sclerosis and Its Models. 2005, 435-449. DOI: 10.1016/b978-012738761-1/50030-4.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisWhite matter injuryAxonal injuryChannel blockersNitric oxideNon-glucocorticoid steroidsCalcium channel blockersHuman multiple sclerosis lesionsSodium channel blockersMultiple sclerosis lesionsEffects of drugsAutoimmune encephalomyelitisMS pathologyOptic nerveMultiple sclerosisFunctional outcomeNeuroprotective agentsΓ-aminobutyric acidHypoxic injuryPathological evidenceSpinal nervesSpinal cordAdrenergic receptorsVivo preparationSclerosis lesions19 Molecular Mechanisms of Calcium Influx in Axonal Degeneration
Stys P, Waxman S. 19 Molecular Mechanisms of Calcium Influx in Axonal Degeneration. 2005, 275-292. DOI: 10.1016/b978-012738761-1/50020-1.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisAxonal degenerationMultiple sclerosisAxonal injuryCalcium influxInflammatory central nervous system disordersCentral nervous system disordersAcute axonal injuryPotential neuroprotective strategiesWhite matter injuryCellular calcium overloadNervous system disordersAutoimmune encephalomyelitisAxonal damageNeuroprotective strategiesGlutamate releasePathophysiological mechanismsCa overloadCalcium overloadSystem disordersInadequate deliveryMyelinated axonsAberrant operationNitric oxideCa channels7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models
Waxman S. 7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models. 2005, 101-118. DOI: 10.1016/b978-012738761-1/50008-0.Peer-Reviewed Original ResearchMultiple sclerosisSodium channel subtypesVoltage-gated sodium channelsSodium channelsChannel subtypesDistinct voltage-gated sodium channelsPathophysiology of MSAxonal degenerationTherapeutic strategiesSclerosisFiring patternsExperimental modelMaladaptive roleNeuronal signalingSubtypesMolecular analysisAltered distributionNeuronsRecent studiesMajor contributorPathophysiologyAxonsDegenerationDiseaseImportant role
2004
Chapter 41 Ischemic White Matter Damage
Stys P, Waxman S. Chapter 41 Ischemic White Matter Damage. 2004, 985-1007. DOI: 10.1016/b978-012439510-7/50094-2.Peer-Reviewed Original ResearchIschemic white matter injuryIschemic white matter damageIschemic CNS injuryMore chronic statesWhite matter injuryWhite matter damageMammalian white matterClinical disabilityAcute strokePeriventricular leukomalaciaAxonal disordersCerebral palsyIschemic damageVascular dementiaMultiple sclerosisCNS injuryMatter damageSocioeconomic burdenMyelinated fibersSuccessful therapyChronic stateWhite matterIrreversible compromiseDeleterious eventsWestern populations
2003
Multiple Sclerosis
Vollmer T, Preiningerova J, Waxman S. Multiple Sclerosis. 2003 DOI: 10.1038/npg.els.0000192.Peer-Reviewed Original Research
2002
Axotomy does not up-regulate expression of sodium channel Nav1.8 in Purkinje cells
Black J, Dusart I, Sotelo C, Waxman S. Axotomy does not up-regulate expression of sodium channel Nav1.8 in Purkinje cells. Brain Research 2002, 101: 126-131. PMID: 12007840, DOI: 10.1016/s0169-328x(02)00200-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsAxotomyCerebellumDisease Models, AnimalFemaleGanglia, SpinalGene Expression RegulationImmunohistochemistryMultiple SclerosisNAV1.8 Voltage-Gated Sodium ChannelNeurons, AfferentNeuropeptidesPurkinje CellsRatsRats, WistarRNA, MessengerSodium ChannelsUp-RegulationZebrafish ProteinsConceptsMultiple sclerosisPurkinje cellsSensory neuron-specific sodium channelsDorsal root ganglion neuronsAberrant expressionSodium channelsHuman multiple sclerosisPrimary sensory neuronsSodium channel Nav1.8Specific sodium channelsCerebellar Purkinje cellsGanglion neuronsSensory neuronsAxotomySurgical modelSodium channel transcriptsExperimental modelCerebellar functionChannel transcriptsNeuronsSitu hybridizationCellsExpressionNav1.8Sclerosis
2001
Transcriptional channelopathies: An emerging class of disorders
Waxman S. Transcriptional channelopathies: An emerging class of disorders. Nature Reviews Neuroscience 2001, 2: 652-659. PMID: 11533733, DOI: 10.1038/35090026.Peer-Reviewed Original ResearchConceptsNerve injuryMultiple sclerosisSodium channel geneTranscriptional channelopathiesChannel transcriptionPeripheral nerve injurySpinal sensory neuronsChannel genesExperimental nerve injuryFamily of disordersAction potential conductionAutoimmune channelopathiesDemyelinated nervesNeuropathic painDemyelinating conditionMotor abnormalitiesNeurotrophic factorClass of disordersSensory neuronsCalcium channelsChannel expressionCerebellar ataxiaPurkinje cellsPotential conductionChannelopathies
2000
Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states11Published on the World Wide Web on 15 August 2000.
Waxman S, Dib-Hajj S, Cummins T, Black J. Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states11Published on the World Wide Web on 15 August 2000. Brain Research 2000, 886: 5-14. PMID: 11119683, DOI: 10.1016/s0006-8993(00)02774-8.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsSodium channel gene expressionSodium channel geneChannel gene expressionChannel genesGene expressionPost-transcriptional levelNormal nervous systemSodium channel expressionSodium channelsChannel expressionMolecular plasticityGenesDynamic expressionCell membraneHypothalamic magnocellular neurosecretory neuronsDifferent repertoiresMultiple sclerosisNervous systemTherapeutic opportunitiesSodium channel subtypesExpressionElectrogenic propertiesRegulationChannel subtypesDysregulationSensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis
Black J, Dib-Hajj S, Baker D, Newcombe J, Cuzner M, Waxman S. Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 11598-11602. PMID: 11027357, PMCID: PMC17246, DOI: 10.1073/pnas.97.21.11598.Peer-Reviewed Original ResearchConceptsExperimental allergic encephalomyelitisMultiple sclerosisAllergic encephalomyelitisClinical abnormalitiesChannel expressionPurkinje cellsTrigeminal ganglion neuronsBrains of micePeripheral nervous systemSodium channel expressionIon channel expressionCerebellar Purkinje cellsAbnormal repertoiresAxonal degenerationControl miceGanglion neuronsControl subjectsMouse modelNormal brainAnimal modelsNervous systemNeurological diseasesSodium channelsProtein expressionAbnormal patternsDo ‘demyelinating’ diseases involve more than myelin?
Waxman S. Do ‘demyelinating’ diseases involve more than myelin? Nature Medicine 2000, 6: 738-739. PMID: 10888913, DOI: 10.1038/77450.Peer-Reviewed Original Research
1988
Evoked potentials in suspected multiple sclerosis: Diagnostic value and prediction of clinical course
Hume A, Waxman S. Evoked potentials in suspected multiple sclerosis: Diagnostic value and prediction of clinical course. Journal Of The Neurological Sciences 1988, 83: 191-210. PMID: 3128646, DOI: 10.1016/0022-510x(88)90068-8.Peer-Reviewed Original ResearchConceptsSilent lesionsMultiple sclerosisOptic neuritisIsolated optic neuritisDefinite multiple sclerosisEP abnormalitiesMS suspectsClinical deteriorationBrainstem auditoryClinical courseVisual EPsChance of deteriorationNeurologic disordersOnly abnormalityNormal EPsPatientsAuditory EPsClinical diagnosisDiagnostic valueLesionsSclerosisNeuritisChronicAbnormalitiesFollow