2021
Emerging hiPSC Models for Drug Discovery in Neurodegenerative Diseases
Trudler D, Ghatak S, Lipton S. Emerging hiPSC Models for Drug Discovery in Neurodegenerative Diseases. International Journal Of Molecular Sciences 2021, 22: 8196. PMID: 34360966, PMCID: PMC8347370, DOI: 10.3390/ijms22158196.Peer-Reviewed Original ResearchConceptsAmyotrophic lateral sclerosisNeurodegenerative diseasesParkinson's diseaseAnimal modelsAlzheimer's diseaseEffective disease-modifying therapiesHuntington's diseaseDisease-modifying therapiesSeverity of symptomsHuman samplesHiPSC-derived neural cellsHealthy donorsEffective treatmentLateral sclerosisEconomic burdenHuman-induced pluripotent stem cell (hiPSC) technologyProgressive deteriorationNeural functionDiseaseHiPSC modelsNeural cellsPluripotent stem cell (iPSC) technologyDisease mechanismsPoor accessMillions of people
2009
Excitotoxicity in Neurodegenerative Disease
Haeberlein S, Lipton S. Excitotoxicity in Neurodegenerative Disease. 2009, 77-86. DOI: 10.1016/b978-008045046-9.00498-8.Peer-Reviewed Original ResearchHuman immunodeficiency virus-associated dementiaExcessive glutamate stimulationSpinal cord traumaMajor excitatory neurotransmitterAmyotrophic lateral sclerosisCord traumaExcitatory neurotransmitterGlutamate stimulationLateral sclerosisParkinson's diseaseTherapeutic interventionsAlzheimer's diseaseNeurodegenerative disordersDiseaseNeurodegenerative diseasesDownstream mechanismsHuntington's diseaseExcitotoxicityBrainSclerosisGlaucomaEpilepsyDementiaStrokeNeurotransmitters
2007
CHAPTER 25 Functional Characterization of Neurons
McKerchner S, Talantova M, Lipton S. CHAPTER 25 Functional Characterization of Neurons. 2007, 373-386. DOI: 10.1016/b978-012370465-8/50030-2.Peer-Reviewed Original ResearchCentral nervous systemAmyotrophic lateral sclerosisJuvenile-onset diseaseStem cell therapyNeuronal damageCurative treatmentElectrophysiological criteriaMacular degenerationLysosomal storage diseaseParkinson's diseaseLateral sclerosisOnset diseaseNervous systemAlzheimer's diseaseDiseaseCell therapySuch pathologyHuntington's diseaseStorage diseaseEarly childhoodTotal absenceLabeling cellsSclerosisTherapyInjury
1998
■ REVIEW : Excitotoxicity, Free Radicals, Necrosis, and Apoptosis
Lipton S, Nicotera P. ■ REVIEW : Excitotoxicity, Free Radicals, Necrosis, and Apoptosis. The Neuroscientist 1998, 4: 345-352. DOI: 10.1177/107385849800400516.Peer-Reviewed Original ResearchNitric oxideMajor excitatory neurotransmitterCentral nervous systemFailure of neuronsFree radicalsNeuronal cell culturesActivation of proteasesNeuronal injuryAIDS dementiaNeuronal necrosisInitial insultExcitatory neurotransmitterNervous systemApoptotic death programAlzheimer's diseaseHuntington's diseaseDiseaseInsultExcitotoxicityMitochondrial membrane potentialNecrosisCell deathDeath programNeuronsApoptosis
1995
Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures.
Bonfoco E, Krainc D, Ankarcrona M, Nicotera P, Lipton S. Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures. Proceedings Of The National Academy Of Sciences Of The United States Of America 1995, 92: 7162-7166. PMID: 7638161, PMCID: PMC41299, DOI: 10.1073/pnas.92.16.7162.Peer-Reviewed Original ResearchConceptsForm of neurotoxicityN-methyl-D-aspartate receptor-mediated neurotoxicityCell damageChronic neurologic disordersNeuronal cell damageCortical cell culturesFinal common pathwayNitric oxide/Superoxide dismutaseS-nitrosocysteineAIDS dementiaNecrotic cell damageFocal ischemiaAcute swellingInitial insultCortical neuronsNeurologic disordersAlzheimer's diseaseNitric oxideNMDANeurodegenerative diseasesHuntington's diseaseIntense exposureNeurotoxicityCommon pathway
1994
Actions of redox-related congeners of nitric oxide at the NMDA receptor
Lipton S, Stamler J. Actions of redox-related congeners of nitric oxide at the NMDA receptor. Neuropharmacology 1994, 33: 1229-1233. PMID: 7870283, DOI: 10.1016/0028-3908(94)90021-3.Peer-Reviewed Original ResearchConceptsProtein S-nitrosylationDisulfide bond formationPlasma membraneS-nitrosylationRedox milieuNovel therapeutic strategiesCell functionMechanistic importanceNMDA receptorsNeuroprotective pathwaysSulfhydryl oxidationNMDA receptor activityBiological systemsPathwayReceptor activityFormation of peroxynitriteHuntington's diseaseReceptorsTherapeutic strategiesCongenersNitric oxideTransductionCa2Excessive activationDownregulationCa2+, N-Methyl-d-Aspartate Receptors, and Aids-Related Neuronal Injury
Lipton S. Ca2+, N-Methyl-d-Aspartate Receptors, and Aids-Related Neuronal Injury. International Review Of Neurobiology 1994, 36: 1-27. PMID: 7822116, DOI: 10.1016/s0074-7742(08)60301-3.Peer-Reviewed Original ResearchConceptsN-methyl-D-aspartate (NMDA) receptor-operated channelsN-methyl-D-aspartate receptorsHIV-1 envelope protein gp120Existence of HIVVoltage-dependent Ca2Receptor-operated channelsFuture pharmacological interventionsFinal common pathwayAmyotrophic lateral sclerosisEnvelope protein gp120Demise of neuronsNeuronal injuryAIDS patientsNeuronal susceptibilityPharmacological interventionsProtein gp120Lateral sclerosisParkinson's diseaseMacrophage productionInduces releaseHIVNitric oxideNeurodegenerative diseasesDiseaseHuntington's disease
1993
Delayed administration of memantine prevents N‐methyl‐D‐aspartate receptor‐mediated neurotoxicity
Pellegrini J, Lipton S. Delayed administration of memantine prevents N‐methyl‐D‐aspartate receptor‐mediated neurotoxicity. Annals Of Neurology 1993, 33: 403-407. PMID: 8098195, DOI: 10.1002/ana.410330414.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsN-methyl-D-aspartate receptor-mediated neurotoxicityPotent N-methyl-D-aspartate antagonistNeonatal rat retinal ganglion cellsN-methyl-D-aspartate (NMDA) subtypeN-methyl-D-aspartate antagonistsRat retinal ganglion cellsImmunodeficiency syndrome (AIDS) dementiaAcute neurological conditionsHypoxia/ischemiaChronic neurodegenerative diseasesRetinal ganglion cellsNeuronal cell deathMicroM memantineAntiparkinsonian drugsCentral neuronsGanglion cellsExcessive activationGlutamate receptorsNeurological conditionsNeurodegenerative diseasesHuntington's diseaseNeurotoxicityPrimary culturesDisease
1990
Redox modulation of NMDA receptor-mediated toxicity in mammalian central neurons
Levy D, Sucher N, Lipton S. Redox modulation of NMDA receptor-mediated toxicity in mammalian central neurons. Neuroscience Letters 1990, 110: 291-296. PMID: 1970145, DOI: 10.1016/0304-3940(90)90862-4.Peer-Reviewed Original ResearchConceptsCentral neuronsNMDA receptorsN-methyl-D-aspartate (NMDA) subtypeNMDA receptor-mediated toxicityAmyotrophic lateral sclerosis-ParkinsonismAcute neurological injuryGlutamate-induced deathNMDA receptor sitesSurvival of neuronsRetinal ganglion cellsMammalian central neuronsReceptor-operated channelsChronic degenerative diseasesReceptor-mediated toxicityHypoxia-ischemiaNMDA neurotoxicityDementia complexNeurological injurySimilar pathogenesisGanglion cellsGlutamate receptorsEnhanced killingRedox modulationDegenerative diseasesHuntington's disease
1988
Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801.
Hahn J, Aizenman E, Lipton S. Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801. Proceedings Of The National Academy Of Sciences Of The United States Of America 1988, 85: 6556-6560. PMID: 2901101, PMCID: PMC282012, DOI: 10.1073/pnas.85.17.6556.Peer-Reviewed Original ResearchConceptsAntagonist MK-801MK-801N-methyl-D-aspartate (NMDA) receptor-coupled ion channelsExtracellular Ca2N-methyl-D-aspartate antagonist MK-801Rat retinal ganglion cellsReceptor-coupled ion channelsGlutamate-induced cell deathCentral mammalian neuronsRetinal ganglion cellsElevated extracellular Ca2Severe neurological insultPatch-clamp experimentsDementia complexNeuronal deathCentral neuronsGanglion cellsNeurological insultNeurotoxic effectsAlzheimer's diseaseNeurological disordersDegenerative disordersNerve cellsMammalian neuronsHuntington's disease