2018
Alzheimer's Disease Risk Factor Pyk2 Mediates Amyloid-β-Induced Synaptic Dysfunction and Loss
Salazar SV, Cox TO, Lee S, Brody AH, Chyung AS, Haas LT, Strittmatter SM. Alzheimer's Disease Risk Factor Pyk2 Mediates Amyloid-β-Induced Synaptic Dysfunction and Loss. Journal Of Neuroscience 2018, 39: 758-772. PMID: 30518596, PMCID: PMC6343652, DOI: 10.1523/jneurosci.1873-18.2018.Peer-Reviewed Original ResearchConceptsTransgenic AD model miceAD model miceAbsence of Pyk2Synaptic dysfunctionModel miceHippocampal slicesSynaptic transmissionAlzheimer's diseaseAmyloid-β plaque pathologyHippocampal Schaffer collateral pathwayDisease riskLearning/memory deficitsDeletion of Pyk2Suppression of LTPBasal synaptic transmissionLate-onset Alzheimer's diseaseImpairment of learningSchaffer collateral pathwayAD-related synaptic dysfunctionAlzheimer's disease riskLate-onset Alzheimer's disease (LOAD) riskOnset Alzheimer's diseaseAge-dependent lossMechanism of actionSynaptic LTD
2015
Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models*
Kostylev MA, Kaufman AC, Nygaard HB, Patel P, Haas LT, Gunther EC, Vortmeyer A, Strittmatter SM. Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models*. Journal Of Biological Chemistry 2015, 290: 17415-17438. PMID: 26018073, PMCID: PMC4498078, DOI: 10.1074/jbc.m115.643577.Peer-Reviewed Original ResearchAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBehavior, AnimalDisease Models, AnimalFemaleHumansMaleMemory DisordersMiceMice, Inbred C57BLMice, Mutant StrainsMice, TransgenicMiddle AgedMolecular WeightPrefrontal CortexPresenilin-1PrionsProtein Structure, QuaternaryPrPC ProteinsRecombinant ProteinsFyn inhibition rescues established memory and synapse loss in Alzheimer mice
Kaufman AC, Salazar SV, Haas LT, Yang J, Kostylev MA, Jeng AT, Robinson SA, Gunther EC, van Dyck CH, Nygaard HB, Strittmatter SM. Fyn inhibition rescues established memory and synapse loss in Alzheimer mice. Annals Of Neurology 2015, 77: 953-971. PMID: 25707991, PMCID: PMC4447598, DOI: 10.1002/ana.24394.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseTransgenic miceGlu receptorsAPP/PS1 transgenic miceAPP/PS1 miceMemory deficitsEffective disease-modifying agentsAD mouse modelPS1 transgenic miceAD transgenic miceDisease-modifying agentsTau transgenic miceWeeks of treatmentPrecursor protein metabolismSpatial memory deficitsNovel object recognitionMorris water mazeBrain slice assaysAZD0530 treatmentMicroglial activationPS1 miceVehicle treatmentSynapse lossAlzheimer's miceAD pathology
2012
LRRTM1-deficient mice show a rare phenotype of avoiding small enclosures—A tentative mouse model for claustrophobia-like behaviour
Voikar V, Kulesskaya N, Laakso T, Lauren J, Strittmatter SM, Airaksinen MS. LRRTM1-deficient mice show a rare phenotype of avoiding small enclosures—A tentative mouse model for claustrophobia-like behaviour. Behavioural Brain Research 2012, 238: 69-78. PMID: 23089646, PMCID: PMC3784023, DOI: 10.1016/j.bbr.2012.10.013.Peer-Reviewed Original Research
2010
Nogo Receptor Deletion and Multimodal Exercise Improve Distinct Aspects of Recovery in Cervical Spinal Cord Injury
Harel NY, Song KH, Tang X, Strittmatter SM. Nogo Receptor Deletion and Multimodal Exercise Improve Distinct Aspects of Recovery in Cervical Spinal Cord Injury. Journal Of Neurotrauma 2010, 27: 2055-2066. PMID: 20809785, PMCID: PMC2978056, DOI: 10.1089/neu.2010.1491.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalExercise TherapyFemaleGene DeletionGenotypeGPI-Linked ProteinsHand StrengthImmunohistochemistryMaleMiceMice, Inbred C57BLMyelin ProteinsNeuronal PlasticityNogo Receptor 1Physical Conditioning, AnimalPostural BalanceReceptors, Cell SurfaceReproducibility of ResultsSerotoninSpinal CordSpinal Cord InjuriesWalkingConceptsSpinal cord injuryCord injuryCervical spinal cord injuryIncomplete spinal cord injuryCervical spinal injurySignificant histological differencesMultimodal exerciseExercise trainingLateral hemisectionReceptor deletionSpinal injuryLesion modelMouse modelAdult miceLesion sizeGene deletionHistological differencesNeural plasticityMild deficitsHistological analysisTraining regimenInjuryPhysical interventionsC3-C4MiceCombination of NEP 1-40 Treatment and Motor Training Enhances Behavioral Recovery After a Focal Cortical Infarct in Rats
Fang PC, Barbay S, Plautz EJ, Hoover E, Strittmatter SM, Nudo RJ. Combination of NEP 1-40 Treatment and Motor Training Enhances Behavioral Recovery After a Focal Cortical Infarct in Rats. Stroke 2010, 41: 544-549. PMID: 20075346, PMCID: PMC2853474, DOI: 10.1161/strokeaha.109.572073.Peer-Reviewed Original ResearchConceptsMotor trainingWeeks postinfarctBehavioral recoverySkilled reachWeek 2Focal cortical infarctsFocal cortical ischemiaFocal ischemic infarctTreatment week 2Foot-fault testFocal ischemic injuryWeeks of treatmentSkilled reach taskNEP 1Cortical infarctsForelimb impairmentCortical ischemiaFoot faultsMotor recoveryIschemic infarctIschemic injuryMotor cortexEndothelin-1Intraventricular infusionMotor function
2009
Rho-Associated Kinase II (ROCKII) Limits Axonal Growth after Trauma within the Adult Mouse Spinal Cord
Duffy P, Schmandke A, Schmandke A, Sigworth J, Narumiya S, Cafferty WB, Strittmatter SM. Rho-Associated Kinase II (ROCKII) Limits Axonal Growth after Trauma within the Adult Mouse Spinal Cord. Journal Of Neuroscience 2009, 29: 15266-15276. PMID: 19955379, PMCID: PMC2855556, DOI: 10.1523/jneurosci.4650-09.2009.Peer-Reviewed Original ResearchMeSH KeywordsAmidesAnalysis of VarianceAnimalsAxonsBehavior, AnimalBrain InjuriesCA1 Region, HippocampalCells, CulturedCholera ToxinEnzyme InhibitorsGanglia, SpinalGene Expression RegulationMedian NeuropathyMiceMice, Inbred C57BLMice, KnockoutMyelin ProteinsNerve RegenerationNeuronsNogo ProteinsPyridinesReceptors, Calcitonin Gene-Related PeptideRhizotomyRho-Associated KinasesSpinal Cord InjuriesTime FactorsVersicansConceptsSpinal cordCNS traumaFunctional recoveryBasso Mouse Scale scoresSpinal Cord Injury StudyAxonal growthDorsal root entry zoneDorsal root ganglion neuronsAdult mouse spinal cordAxonal growth inhibitorsSpinal cord hemisectionRoot entry zoneSpinal cord injuryCaudal spinal cordMouse spinal cordDorsal hemisectionRaphespinal axonsDorsal rhizotomyCrush injuryCord hemisectionCorticospinal axonsChondroitin sulfate proteoglycanCord injuryGanglion neuronsInjury paradigmsLGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology
Owuor K, Harel NY, Englot DJ, Hisama F, Blumenfeld H, Strittmatter SM. LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology. Molecular And Cellular Neuroscience 2009, 42: 448-457. PMID: 19796686, PMCID: PMC2783222, DOI: 10.1016/j.mcn.2009.09.008.Peer-Reviewed Original ResearchConceptsNeuronal morphologyAutosomal dominant partial epilepsyCA1 pyramidal neuronsSeizure thresholdSpontaneous seizuresPartial epilepsyPyramidal neuronsDendritic arborizationLGI1PSD-95LGI1 geneEpilepsy genesADAM23ADPEAFADAM22EpilepsyNeurite outgrowthIon channelsBrain genesUnbiased screenAuditory featuresOutgrowthSeizuresArborizationRelated proteins
2008
Nogo-66 Receptor Antagonist Peptide (NEP1-40) Administration Promotes Functional Recovery and Axonal Growth After Lateral Funiculus Injury in the Adult Rat
Cao Y, Shumsky JS, Sabol MA, Kushner RA, Strittmatter S, Hamers FP, Lee DH, Rabacchi SA, Murray M. Nogo-66 Receptor Antagonist Peptide (NEP1-40) Administration Promotes Functional Recovery and Axonal Growth After Lateral Funiculus Injury in the Adult Rat. Neurorehabilitation And Neural Repair 2008, 22: 262-278. PMID: 18056009, PMCID: PMC2853251, DOI: 10.1177/1545968307308550.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalDenervationEfferent PathwaysFemaleGPI-Linked ProteinsGrowth ConesMyelin ProteinsNerve RegenerationNeuronal PlasticityNogo Receptor 1Peptide FragmentsPyramidal TractsRaphe NucleiRatsRats, Sprague-DawleyReceptors, Cell SurfaceRecovery of FunctionRed NucleusSpinal Cord InjuriesSpinal Nerve RootsTreatment OutcomeWallerian DegenerationConceptsNEP1-40 groupDorsal root axonsRST axonsRubrospinal axonsRubrospinal tractAxonal growthNEP1-40 treatmentPromotes Functional RecoveryCervical spinal cordDorsal hemisectionForelimb usageNEP1-40Corticospinal axonsFunctional recoveryIntrathecal deliveryLateral funiculusSpinal cordMotor functionOutcome measuresAdult ratsLesion siteOperated controlsWhite matterGait analysisAxons
2006
The Nogo–Nogo Receptor Pathway Limits a Spectrum of Adult CNS Axonal Growth
Cafferty WB, Strittmatter SM. The Nogo–Nogo Receptor Pathway Limits a Spectrum of Adult CNS Axonal Growth. Journal Of Neuroscience 2006, 26: 12242-12250. PMID: 17122049, PMCID: PMC2848954, DOI: 10.1523/jneurosci.3827-06.2006.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAxonsBehavior, AnimalCalcitonin Gene-Related PeptideCentral Nervous SystemFunctional LateralityGlial Fibrillary Acidic ProteinMiceMice, Inbred C57BLMice, KnockoutMyelin Basic ProteinMyelin ProteinsNogo ProteinsProtein Kinase CPsychomotor PerformancePyramidal TractsReceptors, PeptideSignal TransductionConceptsAxonal growthCST regenerationSpinal cord dorsal hemisectionCervical gray matterRole of NogoCorticospinal tract axonsNogo-66 receptorVivo pharmacological studiesFine motor skillsDorsal hemisectionAffected forelimbCST axonsLesion modelUnilateral pyramidotomyGray matterPharmacological studiesReceptor pathwayNogoConflicting resultsMiceMotor skillsAxonsDifferent tractsGenetic assessmentPyramidotomy
2005
Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury
Ji B, Li M, Budel S, Pepinsky RB, Walus L, Engber TM, Strittmatter SM, Relton JK. Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury. European Journal Of Neuroscience 2005, 22: 587-594. PMID: 16101740, PMCID: PMC2846292, DOI: 10.1111/j.1460-9568.2005.04241.x.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAxonsBehavior, AnimalBiotinCells, CulturedChick EmbryoDextransDisease Models, AnimalDose-Response Relationship, DrugDrug InteractionsDrug Therapy, CombinationExploratory BehaviorFemaleGanglia, SpinalGPI-Linked ProteinsImmunoglobulin GLaminectomyMethylprednisoloneMyelin ProteinsMyelin SheathNerve RegenerationNeuronsNogo Receptor 1Pyramidal TractsRatsRats, Long-EvansReceptors, Cell SurfaceReceptors, PeptideRecombinant ProteinsRecovery of FunctionSpinal Cord InjuriesConceptsSpinal cord injuryCord injuryRat spinal cord injuryMP treatmentAdult central nervous systemThoracic dorsal hemisectionNovel experimental therapiesCorticospinal tract axonsRecovery of functionNogo-66 receptorNumber of axonsCentral nervous systemGrowth inhibitory effectsDorsal hemisectionBBB scoresAxonal sproutingFunctional recoveryBresnahan (BBB) scoringAxonal regenerationMotor neuronsExperimental therapiesMethylprednisoloneSynthetic glucocorticoidNervous systemAxonal growth
2004
Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury
Kim JE, Liu BP, Park JH, Strittmatter SM. Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury. Neuron 2004, 44: 439-451. PMID: 15504325, DOI: 10.1016/j.neuron.2004.10.015.Peer-Reviewed Original ResearchMeSH Keywords5,7-DihydroxytryptamineAnimalsAxonsBehavior, AnimalBlotting, NorthernBlotting, SouthernBrainCell CountCells, CulturedCloning, MolecularCornified Envelope Proline-Rich ProteinsDesipramineDisease Models, AnimalEvoked Potentials, MotorFemaleGanglia, SpinalGlial Fibrillary Acidic ProteinGlucoseGPI-Linked ProteinsGrowth ConesImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutMotor ActivityMyelin ProteinsMyelin SheathMyelin-Associated GlycoproteinNerve RegenerationNeuronsNogo ProteinsNogo Receptor 1Phospholipid EthersProteinsPyramidal TractsReceptors, Cell SurfaceRecovery of FunctionSerotoninSerotonin AgentsSpinal CordSpinal Cord InjuriesTime FactorsConceptsAdult CNSNogo-66Spinal cord injuryAdult mammalian CNSNogo-66 receptorDorsal hemisectionDRG neuronsFunctional recoveryRubrospinal fibersCord injuryMyelin inhibitorsComplete transectionCorticospinal fibersMotor functionSpinal cordMotor impairmentAxon regenerationMammalian CNSAxonal growthAxonal outgrowthCNS myelinMiceInhibitory proteinInjuryGrowth conesNeonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity
Weiss J, Takizawa B, McGee A, Stewart WB, Zhang H, Ment L, Schwartz M, Strittmatter S. Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity. Experimental Neurology 2004, 189: 141-149. PMID: 15296844, DOI: 10.1016/j.expneurol.2004.05.018.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornAxonsBehavior, AnimalBiotinCentral Nervous SystemDextransDisease Models, AnimalExploratory BehaviorHumansHypoxia, BrainImmunoblottingImmunohistochemistryInfant, NewbornInfant, PrematureMiceMice, Inbred C57BLMyelin Basic ProteinMyelin ProteinsMyelin-Associated GlycoproteinNogo ProteinsOligodendrogliaReceptors, Cell SurfaceTime FactorsConceptsChronic sublethal hypoxiaPeriventricular leukomalaciaMyelin associated glycoproteinCorticospinal tractWhite matterLow birth weight infantsCerebral white matter volumeBirth weight infantsLow birth weightAnterograde axonal tracingPeriventricular white matterPremature human infantsCNS white matterWhite matter volumeHypoxia-induced reductionWeight infantsAxonal sproutingCerebral ventriculomegalyCorticofugal fibersLocomotor hyperactivityNeonatal hypoxiaPersistent abnormalitiesMotor cortexBirth weightHuman prematurityNogo Receptor Antagonism Promotes Stroke Recovery by Enhancing Axonal Plasticity
Lee JK, Kim JE, Sivula M, Strittmatter SM. Nogo Receptor Antagonism Promotes Stroke Recovery by Enhancing Axonal Plasticity. Journal Of Neuroscience 2004, 24: 6209-6217. PMID: 15240813, PMCID: PMC6729662, DOI: 10.1523/jneurosci.1643-04.2004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBehavior, AnimalDisease Models, AnimalGPI-Linked ProteinsInfarction, Middle Cerebral ArteryMaleMiceMice, KnockoutMyelin ProteinsNeuronal PlasticityNogo ProteinsNogo Receptor 1RatsRats, Sprague-DawleyReceptors, Cell SurfaceReceptors, PeptideRecombinant Fusion ProteinsRecovery of FunctionStrokeTreatment OutcomeConceptsAxonal plasticityStroke recoveryIpsilateral cervical spinal cordMiddle cerebral artery occlusionFocal brain infarctionCerebral artery occlusionCervical spinal cordComplex motor functionContralateral red nucleusUndamaged cortexBrain infarctionArtery occlusionIschemic strokeAxonal sproutingIntracerebroventricular administrationArterial occlusionPharmacological blockadeMotor functionSpinal cordControl animalsRed nucleusAxonal connectionsBehavioral improvementMutant miceStroke
2003
Delayed Systemic Nogo-66 Receptor Antagonist Promotes Recovery from Spinal Cord Injury
Li S, Strittmatter SM. Delayed Systemic Nogo-66 Receptor Antagonist Promotes Recovery from Spinal Cord Injury. Journal Of Neuroscience 2003, 23: 4219-4227. PMID: 12764110, PMCID: PMC6741116, DOI: 10.1523/jneurosci.23-10-04219.2003.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAxonsAxotomyBehavior, AnimalCornified Envelope Proline-Rich ProteinsFemaleGanglia, SpinalGPI-Linked ProteinsInjections, SubcutaneousIntralaminar Thalamic NucleiMembrane ProteinsMiceMice, Inbred C57BLMolecular Sequence DataMolecular WeightMotor ActivityMyelin ProteinsNerve FibersNerve RegenerationNogo Receptor 1Peptide FragmentsProtein BiosynthesisProteinsPyramidal TractsReceptors, Cell SurfaceSerotoninSpinal CordSpinal Cord InjuriesConceptsSpinal cord injuryCord injuryCorticospinal axonsThoracic spinal cord injuryTherapeutic time windowSpinal cord hemisectionSpinal cord traumaCorticospinal tract axonsAdult mammalian CNSNogo-66 receptorOligodendrocyte myelin glycoproteinCNS axonal injuryCord lesionsSubcutaneous treatmentSystemic therapyCord hemisectionCord traumaIntrathecal applicationLocal therapyLocomotor recoveryFunctional recoverySerotonergic fibersAxonal injuryReceptor antagonistAxon sprouting