2019
Limiting Neuronal Nogo Receptor 1 Signaling during Experimental Autoimmune Encephalomyelitis Preserves Axonal Transport and Abrogates Inflammatory Demyelination
Lee JY, Kim MJ, Thomas S, Oorschot V, Ramm G, Aui PM, Sekine Y, Deliyanti D, Wilkinson-Berka J, Niego B, Harvey AR, Theotokis P, McLean C, Strittmatter SM, Petratos S. Limiting Neuronal Nogo Receptor 1 Signaling during Experimental Autoimmune Encephalomyelitis Preserves Axonal Transport and Abrogates Inflammatory Demyelination. Journal Of Neuroscience 2019, 39: 5562-5580. PMID: 31061088, PMCID: PMC6616297, DOI: 10.1523/jneurosci.1760-18.2019.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsAxonal TransportAxonsCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansIntercellular Signaling Peptides and ProteinsKinesinsMaleMiceMice, Inbred C57BLMiddle AgedMyelin SheathNerve Tissue ProteinsNogo Receptor 1Retinal Ganglion CellsSignal TransductionConceptsExperimental autoimmune encephalomyelitisCollapsin response mediator protein 2Optic nerveAxonal degenerationMultiple sclerosisAxonal vesicular transportAutoimmune encephalomyelitisInflammatory demyelinationAxonal integritySeverity of EAECre deletionAxonal transportRetinal ganglion cell axonsAxonal motor proteinsEAE-induced miceImmune-mediated destructionProgressive multiple sclerosisNeuron-specific deletionNogo receptor 1Ganglion cell axonsAnterograde transportFlx/Response mediator protein 2Adeno-associated virus serotype 2Phosphorylation of CRMP2
2012
Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation
Petratos S, Ozturk E, Azari MF, Kenny R, Lee JY, Magee KA, Harvey AR, McDonald C, Taghian K, Moussa L, Aui P, Siatskas C, Litwak S, Fehlings MG, Strittmatter SM, Bernard CC. Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation. Brain 2012, 135: 1794-1818. PMID: 22544872, PMCID: PMC3589918, DOI: 10.1093/brain/aws100.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnalysis of VarianceAnimalsAntibodiesAxonsCD3 ComplexCell Line, TumorDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression RegulationGlycoproteinsGPI-Linked ProteinsGreen Fluorescent ProteinsHumansImmunoprecipitationIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedMultiple SclerosisMutationMyelin ProteinsMyelin-Oligodendrocyte GlycoproteinNerve DegenerationNerve Tissue ProteinsNeuroblastomaNeurofilament ProteinsNogo Receptor 1Optic NervePeptide FragmentsPhosphorylationReceptors, Cell SurfaceRetinal Ganglion CellsSeverity of Illness IndexSilver StainingSpinal CordTau ProteinsTime FactorsTransduction, GeneticTubulinConceptsExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinMultiple sclerosisAxonal degenerationSpinal cordChronic active multiple sclerosis lesionsOptic nerve axonal degenerationNogo-66 receptor 1CRMP-2Axonal growth inhibitorsCollapsin response mediator protein 2Improved clinical outcomesSpinal cord neuronsRetinal ganglion cellsResponse mediator protein 2Central nervous systemViable therapeutic targetAdeno-associated viral vectorMultiple sclerosis lesionsClinical outcomesOptic nerveCord neuronsOligodendrocyte glycoproteinGanglion cells
2010
Laurén et al. reply
Laurén J, Gimbel D, Nygaard H, Gilbert J, Strittmatter S. Laurén et al. reply. Nature 2010, 466: e4-e5. DOI: 10.1038/nature09218.Peer-Reviewed Original ResearchDisease model miceTransgenic Alzheimer's disease model miceAlzheimer's disease model miceDisease miceModel miceDisease progressionTransgenic Alzheimer's disease miceSpatial learningAlzheimer's disease miceAlzheimer's disease progressionSynapse lossAxonal degenerationEarly deathTransgenic miceCellular prion proteinMicePrion proteinPrPCDeficitsExpression cloningDirect assessmentDegenerationMemory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein
Gimbel DA, Nygaard HB, Coffey EE, Gunther EC, Laurén J, Gimbel ZA, Strittmatter SM. Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein. Journal Of Neuroscience 2010, 30: 6367-6374. PMID: 20445063, PMCID: PMC3323924, DOI: 10.1523/jneurosci.0395-10.2010.Peer-Reviewed Original ResearchConceptsTransgenic miceAlzheimer's diseaseCellular prion proteinSpatial learningAD transgenic miceTransgenic AD modelTransgenic Alzheimer's micePrnp-/- miceAD-related phenotypesAmyloid-beta peptideAbeta accumulationAbeta plaquesAbeta levelsAD micePrion proteinAlzheimer's miceAxonal degenerationAPP expressionSynaptic markersHippocampal slicesDetectable impairmentEarly deathAD modelBehavioral impairmentsMemory impairment