Adjunct Faculty
Adjunct faculty typically have an academic or research appointment at another institution and contribute or collaborate with one or more School of Medicine faculty members or programs.
Adjunct rank detailsStuart Lipton, MD, PhD
Adjunct Professor of NeurologyAbout
Research
Publications
2025
Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice
Lin J, Callender J, Mayfield J, McClatchy D, Ojeda-Juárez D, Pourhamzeh M, Soldau K, Kurt T, Danque G, Khuu H, Ronson J, Pizzo D, Du Y, Gruber M, Sevillano A, Wang J, Orrú C, Chen J, Funk G, Aguilar-Calvo P, Aulston B, Roy S, Rho J, Bui J, Newton A, Lipton S, Caughey B, Patrick G, Doré K, Yates J, Sigurdson C. Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice. Journal Of Clinical Investigation 2025, 135: e186432. PMID: 40185484, PMCID: PMC12077891, DOI: 10.1172/jci186432.Peer-Reviewed Original ResearchConceptsN-methyl-D-aspartate receptorsProtein kinase CAmino terminusPrion proteinN-methyl-D-aspartateMutant prion proteinNMDA receptor activationN-linked glycosylation sitesExcitatory-inhibitory imbalanceHippocampal pyramidal neuronsDownstream signaling eventsActivate protein kinase CNMDAR channelsNeuronal hyperexcitabilityFunctional motifsGlutamate receptorsCalcium influxPhosphoproteomic analysisPyramidal neuronsGlycosylation sitesSignaling eventsReceptor activationPrion-infected miceDendritic beadingSynapse lossdiAcCA, a Pro-Drug for Carnosic Acid That Activates the Nrf2 Transcriptional Pathway, Shows Efficacy in the 5xFAD Transgenic Mouse Model of Alzheimer’s Disease
Banerjee P, Wang Y, Carnevale L, Patel P, Raspur C, Tran N, Zhang X, Natarajan R, Roberts A, Baran P, Lipton S. diAcCA, a Pro-Drug for Carnosic Acid That Activates the Nrf2 Transcriptional Pathway, Shows Efficacy in the 5xFAD Transgenic Mouse Model of Alzheimer’s Disease. Antioxidants 2025, 14: 293. PMID: 40227330, PMCID: PMC11939361, DOI: 10.3390/antiox14030293.Peer-Reviewed Original ResearchAlzheimer's diseaseNrf2 transcriptional pathwayTranscriptional pathwaysAmyloid plaque formationMouse model of Alzheimer's diseaseTransgenic mouse model of Alzheimer's diseaseModel of Alzheimer's diseaseAD transgenic miceCorrelated to cognitive declineNeuritic aggregatesTau tanglesAmyloid plaquesPhospho-tauCarnosic acidSynapse lossHuman ADPurified CATransgenic mouse modelPhenolic diterpenesAmyloidMicroglial inflammationPathwayPlaque formationTransgenic miceNrf2S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity
Zhang X, Vlkolinsky R, Wu C, Dolatabadi N, Scott H, Prikhodko O, Zhang A, Blanco M, Lang N, Piña-Crespo J, Nakamura T, Roberto M, Lipton S. S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2418179122. PMID: 40014571, PMCID: PMC11892585, DOI: 10.1073/pnas.2418179122.Peer-Reviewed Original ResearchConceptsActivity-dependent gene expressionGene expressionAlzheimer's diseaseCREB-dependent gene expressionS-nitrosylationNitric oxide (NO)-related speciesTargets of S-nitrosylationNeuronal activity-dependent gene expressionPathogenesis of ADDecreased neurite lengthIncreased neuronal cell deathNeuronal cell deathSynaptic plasticityTranscriptional pathwaysCell deathCRISPR/Cas9 techniqueTranscription coactivator 1AD modelLong-term memory formationIncreased S-nitrosylationLong-term potentiationTherapeutic targetExpressionNeurite lengthCerebrocortical neuronsInflammaging, Neuroinflammation, and Synaptic Damage in Alzheimer's Disease
Carnevale L, Lipton S. Inflammaging, Neuroinflammation, and Synaptic Damage in Alzheimer's Disease. 2025, 303-314. DOI: 10.1016/b978-0-323-95702-1.00491-7.Peer-Reviewed Original ResearchAmyloid-betaAlzheimer's diseaseAmyloid-beta precursor proteinProteins amyloid-betaNeuronal healthDiscovery of mutationsAlzheimer's disease casesGenome sequencePresenilin-1Precursor proteinProtein functionAlzheimer's disease researchImmune signalingLipid transportProgressive neurodegenerative diseaseAlzheimer's disease patientsGenetic causeApolipoprotein E4Genes related to lipid transportSynaptic damageStress-mediated alterationsNeurodegenerative diseasesDisease pathologyProteinAlzheimer
2024
Redox regulation, protein S-nitrosylation, and synapse loss in Alzheimer’s and related dementias
Oh C, Nakamura T, Zhang X, Lipton S. Redox regulation, protein S-nitrosylation, and synapse loss in Alzheimer’s and related dementias. Neuron 2024, 112: 3823-3850. PMID: 39515322, PMCID: PMC11624102, DOI: 10.1016/j.neuron.2024.10.013.Peer-Reviewed Original ResearchProtein S-nitrosylationS-nitrosylationEndoplasmic reticulumRedox-mediated posttranslational modificationDiseases associated with protein aggregationProtein aggregationSynapse lossModulating protein activityNetwork of proteinsMultiple neurodegenerative disordersUbiquitin-proteasome systemS-nitrosylation reactionPosttranslational modificationsMitochondrial metabolismExcessive nitrosative stressEnzymatic machineryRedox regulationProtein activityProtein networkDysfunction pathwayMicroglial phagocytosisSingle proteinsBioenergetic compromiseReview recent findingsProteinA 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 ResearchDetecting Boolean Asymmetric Relationships With a Loop Counting Technique and its Implications for Analyzing Heterogeneity Within Gene Expression Datasets
Zhou H, Lin W, Labra S, Lipton S, Elman J, Schork N, Rangan A. Detecting Boolean Asymmetric Relationships With a Loop Counting Technique and its Implications for Analyzing Heterogeneity Within Gene Expression Datasets. IEEE Transactions On Computational Biology And Bioinformatics 2024, 22: 27-38. PMID: 39471117, PMCID: PMC12037869, DOI: 10.1109/tcbb.2024.3487434.Peer-Reviewed Original ResearchSubsets of genesGene-gene relationshipsGene expression dataGene-gene interactionsGene expression datasetsRNA-sequencing data setsDetected biclustersExpression datasetsGene pathwaysSubsets of cellsGenesRegulatory effectsBiclusteringCorrelated expressionAsymmetric interactionsSymmetric interactionsInteractionExpressionCellsUsing in vivo intact structure for system-wide quantitative analysis of changes in proteins
Son A, Kim H, Diedrich J, Bamberger C, McClatchy D, Lipton S, Yates J. Using in vivo intact structure for system-wide quantitative analysis of changes in proteins. Nature Communications 2024, 15: 9310. PMID: 39468068, PMCID: PMC11519357, DOI: 10.1038/s41467-024-53582-x.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseProtein footprinting methodGlobal expression profilingIn vivo conformationStructural alterations of proteinsCo-expressed proteinsMass spectrometry-based methodsAlterations of proteinsProteostasis dysfunctionSpectrometry-based methodsProtein misfoldingConformation of proteinsStructural changesLysine residuesDynamic structural changesBiological functionsProteomics experimentsDimethyl labelingExpression profilesProtein conformationConformational changesProteinIntact proteinDesign of therapeutic interventionsMeasuring dynamic structural changesDysregulation of miRNA expression and excitation in MEF2C autism patient hiPSC-neurons and cerebral organoids
Trudler D, Ghatak S, Bula M, Parker J, Talantova M, Luevanos M, Labra S, Grabauskas T, Noveral S, Teranaka M, Schahrer E, Dolatabadi N, Bakker C, Lopez K, Sultan A, Patel P, Chan A, Choi Y, Kawaguchi R, Stankiewicz P, Garcia-Bassets I, Kozbial P, Rosenfeld M, Nakanishi N, Geschwind D, Chan S, Lin W, Schork N, Ambasudhan R, Lipton S. Dysregulation of miRNA expression and excitation in MEF2C autism patient hiPSC-neurons and cerebral organoids. Molecular Psychiatry 2024, 30: 1479-1496. PMID: 39349966, PMCID: PMC11919750, DOI: 10.1038/s41380-024-02761-9.Peer-Reviewed Original ResearchMEF2C haploinsufficiency syndromeLoss-of-function mutationsCerebral organoidsHaploinsufficiency syndromeReceptor antagonistHiPSC-neuronsDecreased neurogenesisSevere formCerebrocortical neuronsAnimal studiesExtrasynaptic activationMEF2CAbnormal phenotypesNeurodevelopmentNeuronsDeficitsOrganoidsTranscription factorsMutationsNitroSynapsinGene networksDysregulation of miRNA expressionSingle‐Cell Patch‐Clamp/Proteomics of Human Alzheimer's Disease iPSC‐Derived Excitatory Neurons Versus Isogenic Wild‐Type Controls Suggests Novel Causation and Therapeutic Targets
Ghatak S, Diedrich J, Talantova M, Bhadra N, Scott H, Sharma M, Albertolle M, Schork N, Yates J, Lipton S. Single‐Cell Patch‐Clamp/Proteomics of Human Alzheimer's Disease iPSC‐Derived Excitatory Neurons Versus Isogenic Wild‐Type Controls Suggests Novel Causation and Therapeutic Targets. Advanced Science 2024, 11: e2400545. PMID: 38773714, PMCID: PMC11304297, DOI: 10.1002/advs.202400545.Peer-Reviewed Original ResearchAbundance of individual proteinsIsogenic wild-type controlsSingle-cell (scHuman AD brainsWild-type controlsSingle-cellAlzheimer's diseaseMulticellular organismsSingle-cell physiologyAD brainTherapeutic targetIndividual proteinsProteomic informationGenetic mutationsProteinProteomicsProtein expressionHiPSC-neuronsExcitatory neuronsElectrophysiological statusDisease statesPhysiologyElectrophysiological dataNeuronsNeuronal level