2025
CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models
Leser F, Júnyor F, Pagnoncelli I, Delgado A, Medeiros I, Nóbrega A, Andrade B, de Lima M, da Silva N, Jacob L, Boyé K, Geraldo L, de Souza A, Maron-Gutierrez T, Castro-Faria-Neto H, Follmer C, Braga C, Neves G, Eichmann A, Romão L, Lima F. CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models. Journal Of Neuroinflammation 2025, 22: 31. PMID: 39894839, PMCID: PMC11789347, DOI: 10.1186/s12974-024-03318-x.Peer-Reviewed Original ResearchConceptsMouse model of PDModel of PDMouse modelDopaminergic neuronsNeuron-microglia communicationNeuron-glia communicationParkinson's diseaseCCR7-dependent mannerMicroglial cell activationCCR7 expressionCCL21-CCR7Progressive degenerative diseaseCCR7 receptorMicroglial cell migrationInflammatory profileChemokine CCL21Cell activationCCL21Therapeutic strategiesChemokine inhibitorsTherapeutic implicationsMicroglial activationReceptor pathwayCCR7Behavioral deficits
2021
Intravenous infusion of mesenchymal stem cells delays disease progression in the SOD1G93A transgenic amyotrophic lateral sclerosis rat model
Magota H, Sasaki M, Kataoka-Sasaki Y, Oka S, Ukai R, Kiyose R, Onodera R, Kocsis JD, Honmou O. Intravenous infusion of mesenchymal stem cells delays disease progression in the SOD1G93A transgenic amyotrophic lateral sclerosis rat model. Brain Research 2021, 1757: 147296. PMID: 33516815, DOI: 10.1016/j.brainres.2021.147296.Peer-Reviewed Original ResearchConceptsBlood-spinal cord barrierQuantitative reverse transcription polymerase chain reactionIntravenous infusionDisease progressionMotor neuronsMSC groupLocomotor functionOpen-field locomotor functionPreservation of microvasculatureHind limb functionCommon clinical featuresEvans blue leakageMotor neuron lossReverse transcription-polymerase chain reactionTranscription-polymerase chain reactionDevastating neurodegenerative diseaseBBB scoringBSCB functionRotarod testingClinical featuresNeuron lossLimb functionNeurotrophic factorCurative strategiesSpinal cord
2020
Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer’s disease via H2O2− production
Chun H, Im H, Kang YJ, Kim Y, Shin JH, Won W, Lim J, Ju Y, Park YM, Kim S, Lee SE, Lee J, Woo J, Hwang Y, Cho H, Jo S, Park JH, Kim D, Kim DY, Seo JS, Gwag BJ, Kim YS, Park KD, Kaang BK, Cho H, Ryu H, Lee CJ. Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer’s disease via H2O2− production. Nature Neuroscience 2020, 23: 1555-1566. PMID: 33199896, DOI: 10.1038/s41593-020-00735-y.Peer-Reviewed Original ResearchConceptsReactive astrocytesAlzheimer's diseaseAPP/PS1 micePathogenesis of ADReactivity of astrocytesBrains of patientsAppropriate experimental modelsGlial activationPS1 miceAstrocytic reactivityBrain atrophyPathological featuresNeuronal deathMonoamine oxidase BPathological hallmarkAD modelPrecise molecular mechanismsAnimal modelsAstrocytesCognitive impairmentPathological contributionExperimental modelDiseaseOxidase BEventual deathLoss- or Gain-of-Function Mutations in ACOX1 Cause Axonal Loss via Different Mechanisms
Chung H, Wangler M, Marcogliese P, Jo J, Ravenscroft T, Zuo Z, Duraine L, Sadeghzadeh S, Li-Kroeger D, Schmidt R, Pestronk A, Rosenfeld J, Burrage L, Herndon M, Chen S, Network M, Shillington A, Vawter-Lee M, Hopkin R, Rodriguez-Smith J, Henrickson M, Lee B, Moser A, Jones R, Watkins P, Yoo T, Mar S, Choi M, Bucelli R, Yamamoto S, Lee H, Prada C, Chae J, Vogel T, Bellen H. Loss- or Gain-of-Function Mutations in ACOX1 Cause Axonal Loss via Different Mechanisms. Neuron 2020, 106: 589-606.e6. PMID: 32169171, PMCID: PMC7289150, DOI: 10.1016/j.neuron.2020.02.021.Peer-Reviewed Original ResearchMeSH KeywordsAcyl-CoA OxidaseAnimalsAxonsDrosophilaHumansMiceMutationNerve DegenerationNeurogliaRatsConceptsSchwann cellsAxonal lossMurine Schwann cellsPrimary Schwann cellsTreatment of fliesLong-chain fatty acid β-oxidation pathwayNeuronal lossGlial lossSynaptic transmissionRate-limiting enzymeDevelopmental delayACOX1Elevated levelsFatty acid β-oxidation pathwayReactive oxygen speciesDifferent mechanismsPupal deathPatientsDominant variantFunction mutationsGliaOxygen speciesTreatmentDe novoCellsThe stress-responsive gene GDPGP1/mcp-1 regulates neuronal glycogen metabolism and survival
Schulz A, Sekine Y, Oyeyemi MJ, Abrams AJ, Basavaraju M, Han SM, Groth M, Morrison H, Strittmatter SM, Hammarlund M. The stress-responsive gene GDPGP1/mcp-1 regulates neuronal glycogen metabolism and survival. Journal Of Cell Biology 2020, 219: e201807127. PMID: 31968056, PMCID: PMC7041677, DOI: 10.1083/jcb.201807127.Peer-Reviewed Original ResearchConceptsNeuronal stress resistanceStress resistanceNovel cellular responsesMouse neuronsVariety of stressesCaenorhabditis elegansC. elegansTranscriptional analysisSingle homologueEnvironmental stressFunctional characterizationCellular responsesCell deathNeuronal cell deathNeuronal glycogenGlycogen metabolismWidespread neuronal cell deathElegansSurvival of animalsTauopathy modelMaladaptive responsesKey roleHomologuesGlycogen levelsKnockdown
2019
Prokaryotic SPHINX replication sequences are conserved in mammalian brain and participate in neurodegeneration
Szigeti‐Buck K, Manuelidis L. Prokaryotic SPHINX replication sequences are conserved in mammalian brain and participate in neurodegeneration. Journal Of Cellular Biochemistry 2019, 120: 17687-17698. PMID: 31231867, DOI: 10.1002/jcb.29035.Peer-Reviewed Original ResearchConceptsCreutzfeldt-Jakob diseaseGuinea pigsMammalian brainSporadic Creutzfeldt-Jakob diseaseOnly excitatory neuronsHippocampal pyramidal neuronsGranule cell layerInternal granule cell layerPancreatic islet cellsPyramidal neuronsSporadic CJDHidden infectionType synapsesExcitatory synapsesExcitatory neuronsMossy fibersPurkinje neuronsProgressive neurodegenerationNeuron synapsesIslet cellsSpecific neuronsWestern blotNeuronsPancreatic exocrine cellsKidney tubulesMolecular layer interneurons shape the spike activity of cerebellar Purkinje cells
Brown A, Arancillo M, Lin T, Catt D, Zhou J, Lackey E, Stay T, Zuo Z, White J, Sillitoe R. Molecular layer interneurons shape the spike activity of cerebellar Purkinje cells. Scientific Reports 2019, 9: 1742. PMID: 30742002, PMCID: PMC6370775, DOI: 10.1038/s41598-018-38264-1.Peer-Reviewed Original ResearchConceptsMolecular layer interneuronsPurkinje cellsGABAergic neurotransmissionSpike firingVesicular GABA transporterClasses of interneuronsPurkinje cell functionCerebellar Purkinje cellsComplex spike firingPurkinje cell activityPurkinje cell simple spike firingInhibitory molecular layer interneuronsConditional genetic approachPurkinje cell simple spikesSynaptic inputsStellate cellsSpike activitySimple spike firingFiring propertiesGABA transporterCell activityInterneuronsSelective depletionCell functionComplex spikes
2017
A deafness mechanism of digenic Cx26 (GJB2) and Cx30 (GJB6) mutations: Reduction of endocochlear potential by impairment of heterogeneous gap junctional function in the cochlear lateral wall
Mei L, Chen J, Zong L, Zhu Y, Liang C, Jones R, Zhao H. A deafness mechanism of digenic Cx26 (GJB2) and Cx30 (GJB6) mutations: Reduction of endocochlear potential by impairment of heterogeneous gap junctional function in the cochlear lateral wall. Neurobiology Of Disease 2017, 108: 195-203. PMID: 28823936, PMCID: PMC5675824, DOI: 10.1016/j.nbd.2017.08.002.Peer-Reviewed Original ResearchConceptsCochlear lateral wallEndocochlear potentialHearing lossGap junctional functionDeafness mechanismLateral wallHeterozygous miceCx30 mutationsHair cell degenerationHomozygous knockout miceJunctional functionHeterozygous mouse modelGap junctionsOrgan of CortiSame gap junctional plaquesEP reductionFrequent causePathological changesMouse modelKnockout miceReceptor currentsCell degenerationNormal hearingHeterozygous mutationsMice
2016
Axon regeneration in C. elegans: Worming our way to mechanisms of axon regeneration
Byrne AB, Hammarlund M. Axon regeneration in C. elegans: Worming our way to mechanisms of axon regeneration. Experimental Neurology 2016, 287: 300-309. PMID: 27569538, PMCID: PMC5136328, DOI: 10.1016/j.expneurol.2016.08.015.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsCaenorhabditis elegansDisease Models, AnimalNerve DegenerationNerve RegenerationNeuronsConceptsC. elegansC. elegans researchC. elegans modelSimple nervous systemMammalian nervous systemConserved genomeElegansElegans modelRegeneration responseAxon regenerationCellular mechanismsRegeneration researchTransparent bodyNervous systemRegenerationGenomeFundamental questionsSpeciesMechanismTechnical advancesRegeneration studiesPotential future directionsA painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels
Rolyan H, Liu S, Hoeijmakers JG, Faber CG, Merkies IS, Lauria G, Black JA, Waxman SG. A painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels. Molecular Pain 2016, 12: 1744806916674472. PMID: 27821467, PMCID: PMC5102167, DOI: 10.1177/1744806916674472.Peer-Reviewed Original ResearchConceptsSmall fiber neuropathySmall-diameter axonsTime-dependent degenerationDorsal root ganglion neuronsNerve fiber injuryNervous system disordersPrevious clinical reportsIntracellular calcium levelsMutant Nav1.7 channelsATP levelsAδ nerve fibersHigh altitude sicknessPainful neuropathyTime-dependent increaseFiber injuryClinical onsetGanglion neuronsOxygen species productionSystem disordersCalcium levelsClinical reportsDistal extremitiesIntracellular Ca2NeuropathyNav1.7 channels
2014
Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1
Patterson VL, Zullo AJ, Koenig C, Stoessel S, Jo H, Liu X, Han J, Choi M, DeWan AT, Thomas JL, Kuan CY, Hoh J. Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1. PLOS ONE 2014, 9: e115789. PMID: 25531304, PMCID: PMC4274161, DOI: 10.1371/journal.pone.0115789.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBehavior, AnimalBlotting, WesternCell ProliferationCerebellumFemaleGTP PhosphohydrolasesHigh-Temperature Requirement A Serine Peptidase 2MaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial ProteinsNerve DegenerationNeuronsParkinson DiseaseReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSequence DeletionSerine EndopeptidasesSignal TransductionConceptsNeural-specific deletionStriatal neuronal lossPostnatal day 18Days of ageNeuronal lossNeurological symptomsParkinson's diseaseMouse modelParkinsonian phenotypeSystemic effectsMitochondrial Opa1Day 18Premature deathMutant miceNeural contributionsMiceCerebellar neurodegenerationKey moleculesStructural anomaliesAbnormal activityAbnormal morphologyCerebellumDiseaseComplete penetranceDeathIntravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats
Suzuki S, Kawamata J, Iwahara N, Matsumura A, Hisahara S, Matsushita T, Sasaki M, Honmou O, Shimohama S. Intravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats. Neuroscience Letters 2014, 584: 276-281. PMID: 25449872, DOI: 10.1016/j.neulet.2014.10.039.Peer-Reviewed Original ResearchConceptsHuman bone marrow-derived mesenchymal stem cellsTherapeutic effectParkinson's diseaseCalcium binding adaptor molecule 1Mesenchymal stem cell administrationSubstantia nigra pars compactaHemi-parkinsonian rat modelParkinsonian model ratsTH-positive neuronsAdaptor molecule 1Anti-inflammatory factorsStem cell administrationNovel therapeutic optionsSham-operated ratsBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsGlial activationPars compactaCell administrationTherapeutic optionsDopaminergic neuronsModel ratsDopaminergic neurodegenerationNovel therapiesRat modelMolecular pathogenesis of polymerase gamma–related neurodegeneration
Tzoulis C, Tran G, Coxhead J, Bertelsen B, Lilleng P, Balafkan N, Payne B, Miletic H, Chinnery P, Bindoff L. Molecular pathogenesis of polymerase gamma–related neurodegeneration. Annals Of Neurology 2014, 76: 66-81. PMID: 24841123, PMCID: PMC4140551, DOI: 10.1002/ana.24185.Peer-Reviewed Original ResearchConceptsPolymerase gamma (POLGPOLG mutationsCause of mitochondrial diseaseAccumulation of mitochondrial DNA deletionsMitochondrial DNA depletionMitochondrial DNA deletionsMitochondrial genomeNeuronal lossDNA depletionDNA deletionsSomatic mutagenesisMicrodissected neuronsFocal neuronal necrosisMitochondrial diseaseEvidence of neuronal lossPoint mutationsCombination of histopathologyMassive neuronal lossStable depletionFrozen brain tissueBiological processesMitochondrial dysfunctionFocal cortical lesionsPOLGMolecular mechanismscAMP-PKA phosphorylation of tau confers risk for degeneration in aging association cortex
Carlyle BC, Nairn AC, Wang M, Yang Y, Jin LE, Simen AA, Ramos BP, Bordner KA, Craft GE, Davies P, Pletikos M, Šestan N, Arnsten AF, Paspalas CD. cAMP-PKA phosphorylation of tau confers risk for degeneration in aging association cortex. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 5036-5041. PMID: 24707050, PMCID: PMC3977284, DOI: 10.1073/pnas.1322360111.Peer-Reviewed Original ResearchConceptsNeurofibrillary tanglesAssociation cortexAlzheimer's diseaseSpine apparatusPhosphorylated tauPattern of neurodegenerationLate-stage diseaseHigh-risk factorsNormal aged miceGenetic rodent modelsPrefrontal association cortexPrimary sensory cortexPrimary visual cortexAge-related increasePyramidal neuronsCorticocortical connectionsAged miceRisk factorsGlutamate synapsesSpine synapsesSelective vulnerabilityRodent modelsDendritic spinesSensory cortexProtein kinase phosphorylationInsulin/IGF1 Signaling Inhibits Age-Dependent Axon Regeneration
Byrne AB, Walradt T, Gardner KE, Hubbert A, Reinke V, Hammarlund M. Insulin/IGF1 Signaling Inhibits Age-Dependent Axon Regeneration. Neuron 2014, 81: 561-573. PMID: 24440228, PMCID: PMC3924874, DOI: 10.1016/j.neuron.2013.11.019.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsDisease Models, AnimalForkhead Transcription FactorsGene Expression RegulationGreen Fluorescent ProteinsHumansImmunosuppressive AgentsInsulinInsulin-Like Growth Factor INerve DegenerationNerve RegenerationPhosphotransferases (Alcohol Group Acceptor)PTEN PhosphohydrolaseSignal TransductionSirolimusTime FactorsTranscription Factors
2013
Sodium Channels Contribute to Degeneration of Dorsal Root Ganglion Neurites Induced by Mitochondrial Dysfunction in an In Vitro Model of Axonal Injury
Persson AK, Kim I, Zhao P, Estacion M, Black JA, Waxman SG. Sodium Channels Contribute to Degeneration of Dorsal Root Ganglion Neurites Induced by Mitochondrial Dysfunction in an In Vitro Model of Axonal Injury. Journal Of Neuroscience 2013, 33: 19250-19261. PMID: 24305821, PMCID: PMC6618782, DOI: 10.1523/jneurosci.2148-13.2013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsAxotomyCell DeathCells, CulturedGanglia, SpinalHumansHydrogen PeroxideImmunohistochemistryMiceMice, TransgenicMicrotubulesMitochondrial DiseasesNerve DegenerationNeuritesOxidantsRotenoneSodium Channel BlockersSodium ChannelsSodium-Calcium ExchangerSodium-Potassium-Exchanging ATPaseTetrodotoxinThioureaUncoupling AgentsConceptsAxonal degenerationNeurite degenerationSodium channelsKB-R7943Mouse peripheral sensory neuronsRotenone-induced mitochondrial dysfunctionOxidative stressMitochondrial dysfunctionPeripheral sensory neuronsDorsal root gangliaPeripheral nervous systemDegeneration of neuritesMitochondrial functionVoltage-gated sodium channelsMultiple neurodegenerative disordersSodium-calcium exchangerImpaired mitochondrial functionInjurious cascadeAxonal injuryActivity blockadeRoot gangliaAxonal neuropathySensory neuronsNCX activityDysfunctional intracellularSevere nigrostriatal degeneration without clinical parkinsonism in patients with polymerase gamma mutations
Tzoulis C, Tran G, Schwarzlmüller T, Specht K, Haugarvoll K, Balafkan N, Lilleng P, Miletic H, Biermann M, Bindoff L. Severe nigrostriatal degeneration without clinical parkinsonism in patients with polymerase gamma mutations. Brain 2013, 136: 2393-2404. PMID: 23625061, DOI: 10.1093/brain/awt103.Peer-Reviewed Original ResearchConceptsMitochondrial DNA abnormalitiesPolymerase gamma-encephalopathyCatalytic subunit of polymerase gammaMitochondrial diseaseCopy number of mitochondrial DNAMitochondrial DNA homeostasisDNA abnormalitiesMitochondrial quality controlPolymerase gamma mutationDopamine transporter imagingComplex I deficiencyLevels of deletionIn vivo functional studiesPositron emission tomographyPathogenesis of neurodegenerationMitochondrial DNADNA homeostasisSubstantia nigraPolymerase gammaCatalytic subunitNeurons of patientsRespiratory chainCopy numberClinical parkinsonismGamma mutationsRecessive loss of function of the neuronal ubiquitin hydrolase UCHL1 leads to early-onset progressive neurodegeneration
Bilguvar K, Tyagi NK, Ozkara C, Tuysuz B, Bakircioglu M, Choi M, Delil S, Caglayan AO, Baranoski JF, Erturk O, Yalcinkaya C, Karacorlu M, Dincer A, Johnson MH, Mane S, Chandra SS, Louvi A, Boggon TJ, Lifton RP, Horwich AL, Gunel M. Recessive loss of function of the neuronal ubiquitin hydrolase UCHL1 leads to early-onset progressive neurodegeneration. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 3489-3494. PMID: 23359680, PMCID: PMC3587195, DOI: 10.1073/pnas.1222732110.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge of OnsetAmino Acid SequenceBase SequenceChild, PreschoolExomeFemaleGenes, RecessiveHomozygoteHumansHydrolysisMaleModels, MolecularMolecular Sequence DataMutation, MissenseNerve DegenerationNeuronsPedigreeProtein BindingSequence Analysis, DNASubstrate SpecificitySyndromeThermodynamicsUbiquitinUbiquitin ThiolesteraseConceptsUbiquitin C-terminal hydrolase L1Upper motor neuron dysfunctionMotor neuron dysfunctionProgressive neurodegenerative syndromeEarly-onset progressive neurodegenerationChildhood-onset blindnessWhole-exome sequencingNeuron dysfunctionHomozygous missense mutationIndex caseNervous systemProgressive neurodegenerationNeurodegenerative syndromeCerebellar ataxiaHydrolase activityNear complete lossComplete lossAffected individualsConsanguineous unionsMissense mutationsRecessive lossHomozygosity mappingProper positioningReduced affinitySpasticity
2012
Cell degeneration is not a primary causer for Connexin26 (GJB2) deficiency associated hearing loss
Liang C, Zhu Y, Zong L, Lu G, Zhao H. Cell degeneration is not a primary causer for Connexin26 (GJB2) deficiency associated hearing loss. Neuroscience Letters 2012, 528: 36-41. PMID: 22975134, PMCID: PMC3467974, DOI: 10.1016/j.neulet.2012.08.085.Peer-Reviewed Original ResearchConceptsHair cell lossAuditory brainstem responseCell degenerationCell lossNeuron degenerationPostnatal developmentCx26 deficiencyCochlear hair cell lossSpiral ganglion neuron degenerationDevelopment disordersCx26 knockout miceHair cellsHair cell functionOuter hair cellsSG neuronsNonsyndromic hearing lossKO miceBrainstem responseCochlear cellsHearing lossBasal turnMouse modelKnockout miceCongenital deafnessSignificant degenerationLimiting 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
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