2022
Dendritic Spines and Pain Memory
Benson C, King J, Reimer M, Kauer S, Waxman S, Tan A. Dendritic Spines and Pain Memory. The Neuroscientist 2022, 30: 294-314. PMID: 36461773, DOI: 10.1177/10738584221138251.Peer-Reviewed Original ResearchNeuropathic painDendritic spinesSynaptic transmissionSpinal cord dorsal hornForm of painNew therapeutic approachesSurface of neuronsDorsal hornIntractable painDeep laminaePain memoryTherapeutic approachesPainNervous systemNew therapeuticsSpineMillions of peopleInjuryDiseaseRecent studiesReview articlePrevalenceNeuronsImportant role
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 roleBrainMyelin
2006
Mutations in the sodium channel Nav1.7 underlie inherited erythromelalgia
Dib-Hajj S, Rush A, Cummins T, Waxman S. Mutations in the sodium channel Nav1.7 underlie inherited erythromelalgia. Drug Discovery Today Disease Mechanisms 2006, 3: 343-350. DOI: 10.1016/j.ddmec.2006.09.005.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsSympathetic ganglion neuronsDorsal root gangliaHigh-frequency firingSingle action potentialSodium channel Nav1.7Mild thermal stimuliSevere painDRG neuronsPainful conditionsGanglion neuronsRoot gangliaChannel Nav1.7Action potentialsModel diseaseThermal stimuliErythromelalgiaNeuronsMutant channelsFunctional studiesIEMPainGangliaNav1.7MutationsDisease
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 toxinsDemyelinationFactorsPolyneuropathyCytokines7 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
2003
Multiple Sclerosis
Vollmer T, Preiningerova J, Waxman S. Multiple Sclerosis. 2003 DOI: 10.1038/npg.els.0000192.Peer-Reviewed Original Research
2000
Do ‘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
1995
Anoxic/ischemic injury in axons
STYS P, RANSOM B, BLACK J, WAXMAN S. Anoxic/ischemic injury in axons. 1995, 462-479. DOI: 10.1093/acprof:oso/9780195082937.003.0024.Peer-Reviewed Original ResearchNerve fibersNervous systemAnoxic/ischemic injuryPeripheral nervous systemAnoxia/ischemiaCentral nervous systemIschemic injuryPeripheral axonsAction potential propagationAxonsNormal functionPathological statesBiochemical homeostasisTransmembrane ion gradientsCellular energy metabolismInjuryEnergy metabolismPotential propagationSurvivalHuman diseasesMajor mechanismIon gradientsMembrane polarizationIschemiaDisease
1980
Pathophysiology of nerve conduction: relation to diabetic neuropathy.
WAXMAN S. Pathophysiology of nerve conduction: relation to diabetic neuropathy. Annals Of Internal Medicine 1980, 92: 297-301. PMID: 6243892, DOI: 10.7326/0003-4819-92-2-297.Peer-Reviewed Original ResearchConceptsTotal conduction blockProximal-distal gradientClinicopathologic aspectsDiabetic neuropathyClinical deficitsElectrophysiologic variablesNerve diseasePathophysiologic mechanismsNerve conductionConduction blockPathologic basisConduction velocityImpulse conductionTopographic patternsTemporal dispersionNeuropathyNerveDysfunctionPathophysiologyLesionsDisease
1977
The clinical and physiological implications of hepatoma B12-binding proteins.
Waxman S, Liu C, Schreiber C, Helson L. The clinical and physiological implications of hepatoma B12-binding proteins. Cancer Research 1977, 37: 1908-14. PMID: 66988.Peer-Reviewed Original ResearchConceptsCell linesElevated sialyltransferase activityB12 binding capacitySerum B12Hepatocellular carcinomaHepatoma seraSialic acid contentNormal liverHepatoma cell lineB12Previous casesPatientsHepatomaPerfusateSialyltransferase activityLiverSerumPhysiological implicationsChemotherapyCarcinomaNeoplasiaProteinTumorsDisease