1993
The Therapeutic Potential of Neurotrophic Factors in the Treatment of Parkinson's Disease
Lindsay R, Altar C, Cedarbaum J, Hyman C, Wiegand S. The Therapeutic Potential of Neurotrophic Factors in the Treatment of Parkinson's Disease. Experimental Neurology 1993, 124: 103-118. PMID: 8282068, DOI: 10.1006/exnr.1993.1181.Peer-Reviewed Original ResearchConceptsNeurotrophic factorParkinson's diseaseNeurodegenerative disordersTherapeutic agentsNeurodegenerative diseasesFetal nigral graftsTransplantation of neuronsDopamine neurotrophic factorPartial symptomatic reliefDopamine receptor agonistsNeurotrophic growth factorsPotential clinical useHuman neurodegenerative disordersAppropriate neurotransmittersObvious therapeutic strategyNeuronal lossNigral graftsSymptomatic reliefDevelopment of drugsDopaminergic neuronsNeuroprotective agentsSubstantia nigraNeuronal degenerationNeurotrophin familyDopamine neurons
1992
3‐O‐methyldopa administration does not alter fluorodopa transport into the brain
Guttman M, Léger G, Cedarbaum J, Reches A, Woodward W, Evans A, Diksic M, Gjedde A. 3‐O‐methyldopa administration does not alter fluorodopa transport into the brain. Annals Of Neurology 1992, 31: 638-643. PMID: 1514775, DOI: 10.1002/ana.410310611.Peer-Reviewed Original ResearchConceptsChronic L-DOPA therapyAdvanced Parkinson's diseaseL-dopa therapyPositron emission tomographic studiesL-DOPA administrationEmission tomographic studiesPositron emission tomographyL-dopa preparationsParkinsonian patientsPlasma concentrationsCynomolgus monkeysParkinson's diseasePatientsEmission tomographyL-DOPABrainTomographic studiesDiseaseAdministrationInfusionTherapyBlood
1990
Sustained‐release (+)‐PHNO [MK‐458 (HPMC)] in the treatment of Parkinson's disease: Evidence for tolerance to a selective D2‐receptor agonist administered as a long‐acting formulation
Cedarbaum J, Clark M, Toy L, Green‐Parsons A. Sustained‐release (+)‐PHNO [MK‐458 (HPMC)] in the treatment of Parkinson's disease: Evidence for tolerance to a selective D2‐receptor agonist administered as a long‐acting formulation. Movement Disorders 1990, 5: 298-303. PMID: 1979657, DOI: 10.1002/mds.870050407.Peer-Reviewed Original ResearchConceptsMK-458Disease patientsSelective D2 receptor agonistPostsynaptic dopamine receptorsMotor response fluctuationsD2 receptor agonistParkinson's disease patientsSustained-release formAdjunctive therapyD2 agonistDopamine receptorsSinemetParkinson's diseaseAgonistsResponse fluctuationsProgressive lossPatientsWeeksDiseaseDosageReduced sensitivityDaysTherapyReceptorsThe metabolic anatomy of Parkinson's disease: Complementary [18F]fluorodeoxyglucose and [18F]fluorodopa positron emission tomographic studies
Eidelberg D, Moeller JR, Dhawan V, Sidtis JJ, Ginos JZ, Strother SC, Cedarbaum J, Greene P, Fahn S, Rottenberg DA. The metabolic anatomy of Parkinson's disease: Complementary [18F]fluorodeoxyglucose and [18F]fluorodopa positron emission tomographic studies. Movement Disorders 1990, 5: 203-213. PMID: 2117706, DOI: 10.1002/mds.870050304.Peer-Reviewed Original ResearchConceptsPositron emission tomographyPD patientsParkinson's diseaseScaled Subprofile ModelMetabolic anatomyFDOPA uptakeFDG/PETPositron emission tomographic studiesStriatal FDOPA uptakeTypical Parkinson's diseaseOverall disease severityEmission tomographic studiesGait disturbanceTwo-compartment modelBrain uptakePlasma radioactivityClinical measuresMetabolic asymmetryPET scansDisease processMotor asymmetryLeft-right differencesDisease severityEmission tomographySubprofile Model
1986
Mitochondrial dysfunction and spinocerebellar degenerations
Cedarbaum J, Blass J. Mitochondrial dysfunction and spinocerebellar degenerations. Journal Of Molecular Neuroscience 1986, 4: 43-63. PMID: 3520401, DOI: 10.1007/bf02834298.Peer-Reviewed Original ResearchConceptsSpinocerebellar degenerationProminent clinical featureMitochondrial damageMultiple system degenerationClinical featuresPathophysiological mechanismsOlivopontocerebellar atrophyDiffuse diseaseSystem degenerationNervous systemRelated disordersLong axonsObserved pathologyAtaxiaDegenerationMitochondrial dysfunctionSimplified classificationFriedreich's ataxiaCommon mechanism