2024
A pro-drug derivative of carnosic acid activates the Nrf2 transcriptional pathway and shows efficacy in Alzheimer’s disease transgenic mice
Banerjee P, Roberts A, Natajarian R, Baran P, Lipton S. A pro-drug derivative of carnosic acid activates the Nrf2 transcriptional pathway and shows efficacy in Alzheimer’s disease transgenic mice. Free Radical Biology And Medicine 2024, 224: s96. DOI: 10.1016/j.freeradbiomed.2024.10.212.Peer-Reviewed Original Research
2022
Towards development of disease-modifying therapy for Alzheimer's disease using redox chemical biology pathways
Lipton S. Towards development of disease-modifying therapy for Alzheimer's disease using redox chemical biology pathways. Current Opinion In Pharmacology 2022, 66: 102267. PMID: 35870288, PMCID: PMC9509422, DOI: 10.1016/j.coph.2022.102267.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseDisease-modifying therapiesPotential therapeutic efficacySevere side effectsPotential therapeutic targetCerebral organoid modelTranscription factor Nrf2Absence of diseaseNMDA typeGlutamate receptorsDisease processSide effectsTherapeutic targetTransgenic miceTherapeutic efficacyNeurodegenerative disordersNormal tissuesDiseaseFactor Nrf2Organoid modelsProtein S-nitrosylationS-nitrosylationProtein Keap1TherapyNrf2S-Nitrosylation of cathepsin B affects autophagic flux and accumulation of protein aggregates in neurodegenerative disorders
Kim K, Cho E, Eom J, Oh S, Nakamura T, Oh C, Lipton S, Kim Y. S-Nitrosylation of cathepsin B affects autophagic flux and accumulation of protein aggregates in neurodegenerative disorders. Cell Death & Differentiation 2022, 29: 2137-2150. PMID: 35462559, PMCID: PMC9613756, DOI: 10.1038/s41418-022-01004-0.Peer-Reviewed Original ResearchConceptsS-nitrosylationProtein aggregatesAutophagic fluxProtein S-nitrosylationBlocks autophagic fluxCathepsin BCaspase-dependent neuronal apoptosisPosttranslational modificationsProtease cathepsin BEnzymatic functionLysosomal protease cathepsin BCTSB activityChemical inhibitorsCA-074MeHuman AD brainsEnzymatic activityCysteineNeurodegenerative disordersPostmortem human AD brainTransgenic miceNeuronal apoptosisCTSBAccumulationAD pathogenesisAlzheimer's disease
2000
Functional role and therapeutic implications of neuronal caspase-1 and -3 in a mouse model of traumatic spinal cord injury
Li M, Ona V, Chen M, Kaul M, Tenneti L, Zhang X, Stieg P, Lipton S, Friedlander R. Functional role and therapeutic implications of neuronal caspase-1 and -3 in a mouse model of traumatic spinal cord injury. Neuroscience 2000, 99: 333-342. PMID: 10938439, DOI: 10.1016/s0306-4522(00)00173-1.Peer-Reviewed Original ResearchConceptsSpinal cord injuryCord injuryCaspase-1Acute central nervous system insultLesion sizeCentral nervous system insultsTraumatic spinal cord injuryVehicle-treated miceSham-operated miceNervous system insultsCaspase-3Spinal cord samplesNon-neuronal cellsN-benzyloxycarbonyl-ValCaspase-1 activityCaspase-3 expressionCell deathNeurological dysfunctionCord samplesMotor functionTissue injuryMouse modelTherapeutic implicationsTransgenic miceTissue damage
1997
Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice
Le D, Das S, Wang Y, Yoshizawa T, Sasaki Y, Takasu M, Nemes A, Mendelsohn M, Dikkes P, Lipton S, Nakanishi N. Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice. Brain Research 1997, 52: 235-241. PMID: 9495544, DOI: 10.1016/s0169-328x(97)00261-1.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsBrainCell DeathCerebral CortexCrosses, GeneticDisease SusceptibilityFemaleGenetic VariationHeterozygoteIschemic Attack, TransientMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNeocortexNeuronsPolymerase Chain ReactionReceptors, AMPATranscription, GeneticConceptsNeuronal cell deathMiddle cerebral arteryWild-type neuronsTransgenic miceAMPA receptorsCerebral ischemiaFocal ischemiaGluR2 flipExcitatory amino acid receptorsCell deathAcute cerebral ischemiaGlobal cerebral ischemiaAmino acid receptorsAMPAR-mediated currentsGlutamate receptor antagonistsPermanent focal ischemiaGenetic mouse modelsWild-type controlsExcitotoxic damageEAA receptorsLarge infarctionCerebral arteryFocal strokeGlutamate excitotoxicityNeuronal death