2024
Repetitive mild closed-head injury induced synapse loss and increased local BOLD-fMRI signal homogeneity
Markicevic M, Mandino F, Toyonaga T, Cai Z, Fesharaki-Zadeh A, Chen X, Strittmatter S, Lake E. Repetitive mild closed-head injury induced synapse loss and increased local BOLD-fMRI signal homogeneity. Journal Of Neurotrauma 2024, 0 PMID: 39096127, DOI: 10.1089/neu.2024.0095.Peer-Reviewed Original ResearchChronic variable stressRegional homogeneityFunctional brain abnormalitiesSynapse densityMild closed-head injuryClosed-head injuryTraumatic brain injuryTreat traumatic brain injuryNeurobiological alterationsMild head injuryVariable stressBrain abnormalitiesPositron emission tomographyMultimodal studiesSynaptic densityMagnetic resonance imagingBrain imagingBrain injuryInduce synapse lossFMRIInjured miceMouse modelEmission tomographyResonance imagingCompensatory mechanisms
2021
NogoA-expressing astrocytes limit peripheral macrophage infiltration after ischemic brain injury in primates
Boghdadi AG, Spurrier J, Teo L, Li M, Skarica M, Cao B, Kwan WC, Merson TD, Nilsson SK, Sestan N, Strittmatter SM, Bourne JA. NogoA-expressing astrocytes limit peripheral macrophage infiltration after ischemic brain injury in primates. Nature Communications 2021, 12: 6906. PMID: 34824275, PMCID: PMC8617297, DOI: 10.1038/s41467-021-27245-0.Peer-Reviewed Original ResearchConceptsBrain injuryPeripheral macrophage infiltrationIschemic brain injuryAnti-inflammatory responseMajority of astrocytesNeurite outgrowth inhibitory proteinIschemic strokePeripheral macrophagesReactive astrocytesMacrophage infiltrationStroke recoveryAstrocyte clustersMarmoset monkeysVisual cortexAstrocytesNogoASingle-nucleus transcriptomicsInhibitory proteinInjuryStrokeHuman brainInfiltrationCritical rolePrecise functionOligodendrocytes
2020
Chronic head injury promotes tau and amyloid‐beta pathology and accelerates cognitive decline in a humanized knock‐in model of Alzheimer's disease
Chiasseu M, Fesharaki A, Saito T, Saido T, Strittmatter S. Chronic head injury promotes tau and amyloid‐beta pathology and accelerates cognitive decline in a humanized knock‐in model of Alzheimer's disease. Alzheimer's & Dementia 2020, 16 DOI: 10.1002/alz.047623.Peer-Reviewed Original ResearchMild traumatic brain injuryChronic head injuryHead injuryMorris water maze testAmyloid-beta pathologyAccumulation of amyloidAge-matched miceWater maze testTraumatic brain injuryNovel object recognitionProtein gene mutationsEnvironmental risk factorsAlzheimer's disease symptomsIba1 expressionCortical AβAlzheimer pathologyPhospho-tauClinical manifestationsAD pathologyCortical impactorAD pathogenesisRisk factorsBrain injuryApp NLMaze testGene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in
Chiasseu M, Fesharaki-Zadeh A, Saito T, Saido TC, Strittmatter SM. Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in. Neurobiology Of Disease 2020, 145: 105059. PMID: 32858147, PMCID: PMC7572902, DOI: 10.1016/j.nbd.2020.105059.Peer-Reviewed Original ResearchConceptsMild traumatic brain injuryTraumatic brain injuryAlzheimer's diseaseBrain injuryGene-environment interactionsMild closed head injuryMorris water maze testAge-matched wild-type controlsStrong unmet needAccumulation of amyloidAge-matched miceClosed head injuryWater maze testNovel object recognitionPersistent cognitive deficitsProtein gene mutationsIba1 expressionWild-type controlsPhospho-tauClinical manifestationsAD pathologyAD symptomsHead injuryAD pathogenesisRisk factors
2010
Genetic Deletion and Pharmacological Inhibition of Nogo-66 Receptor Impairs Cognitive Outcome after Traumatic Brain Injury in Mice
Hånell A, Clausen F, Björk M, Jansson K, Philipson O, Nilsson LN, Hillered L, Weinreb PH, Lee D, McIntosh TK, Gimbel DA, Strittmatter SM, Marklund N. Genetic Deletion and Pharmacological Inhibition of Nogo-66 Receptor Impairs Cognitive Outcome after Traumatic Brain Injury in Mice. Journal Of Neurotrauma 2010, 27: 1297-1309. PMID: 20486800, PMCID: PMC2942864, DOI: 10.1089/neu.2009.1255.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryMossy fiber sproutingSoluble NgR1Fiber sproutingBrain injuryCortical impact injury modelEarly post-injury periodNogo-66 receptor 1Hippocampal mossy fiber sproutingBehavioral recovery processSham-injured animalsBrain-injured animalsPost-injury periodSpinal cord injuryOligodendrocyte myelin glycoproteinPharmacological neutralizationBehavioral recoveryFunctional recoveryLoss of tissueCord injuryTimm stainInjury modelMotor functionRodent modelsHistological effects
2009
Axon Regeneration in the Peripheral and Central Nervous Systems
Huebner EA, Strittmatter SM. Axon Regeneration in the Peripheral and Central Nervous Systems. Results And Problems In Cell Differentiation 2009, 48: 305-360. PMID: 19582408, PMCID: PMC2846285, DOI: 10.1007/400_2009_19.Peer-Reviewed Original ResearchConceptsCentral nervous systemPeripheral nervous systemSpinal cord injuryNervous systemAxon regenerationLong-distance axon regenerationMature mammalian central nervous systemMammalian peripheral nervous systemSubstantial functional recoveryMammalian central nervous systemTraumatic brain injuryIntrinsic growth capacityFunctional recoveryCord injuryAxonal disconnectionFunctional deficitsBrain injuryRelated conditionsInjuryRegenerative successExtracellular moleculesGrowth capacityStrokeInosine Alters Gene Expression and Axonal Projections in Neurons Contralateral to a Cortical Infarct and Improves Skilled Use of the Impaired Limb
Zai L, Ferrari C, Subbaiah S, Havton LA, Coppola G, Strittmatter S, Irwin N, Geschwind D, Benowitz LI. Inosine Alters Gene Expression and Axonal Projections in Neurons Contralateral to a Cortical Infarct and Improves Skilled Use of the Impaired Limb. Journal Of Neuroscience 2009, 29: 8187-8197. PMID: 19553458, PMCID: PMC2856695, DOI: 10.1523/jneurosci.0414-09.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBrain InfarctionCerebral CortexComplement C1qComplement C3Disease Models, AnimalExtremitiesFunctional LateralityGene Expression RegulationHeat-Shock ProteinsImmunohistochemistryInjections, IntraventricularInosineNeuronsOligonucleotide Array Sequence AnalysisProteasome Endopeptidase ComplexRatsRats, Sprague-DawleyRecovery of FunctionRNA, MessengerTreatment OutcomeUbiquitinationConceptsUndamaged neuronsSpinal cordSynaptic bouton-like structuresImpaired limbAlters gene expressionCorticospinal tract axonsSpecific cortical areasBouton-like structuresCortical infarctsCorticospinal neuronsDenervated sideUnaffected hemisphereAxon collateralsSensorimotor cortexBrain damageBrain injuryInjury modelLaser capture microdissectionAxonal projectionsGene expressionCortical areasDenervated halfComplement cascadeNeuronsAxon growthFunctional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice
Marklund N, Morales D, Clausen F, Hånell A, Kiwanuka O, Pitkänen A, Gimbel DA, Philipson O, Lannfelt L, Hillered L, Strittmatter SM, McIntosh TK. Functional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice. Neuroscience 2009, 163: 540-551. PMID: 19555742, PMCID: PMC2756649, DOI: 10.1016/j.neuroscience.2009.06.042.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryHemispheric tissue lossNeurological motor functionWT miceBrain injuryMotor functionCortical impact (CCI) TBILittermate controlsAge-matched wild-type littermate controlsMyelin stainingTissue lossMWM taskWild-type littermate controlsCortical lesion volumeAxonal growth inhibitorsRole of NogoMyelin-derived inhibitorAbsence of NogoNeurological motorPoor prognosisFunctional outcomeHemispheric tissuePathophysiological responsesWT littermatesDeficient mice
2006
Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat
Marklund N, Fulp CT, Shimizu S, Puri R, McMillan A, Strittmatter SM, McIntosh TK. Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat. Experimental Neurology 2006, 197: 70-83. PMID: 16321384, PMCID: PMC2849132, DOI: 10.1016/j.expneurol.2005.08.029.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternBrainBrain InjuriesCell CountCornified Envelope Proline-Rich ProteinsDensitometryFunctional LateralityGPI-Linked ProteinsHippocampusImmunohistochemistryMaleMembrane ProteinsMicrotubule-Associated ProteinsMyelin ProteinsNogo ProteinsNogo Receptor 1OligodendrogliaRatsRats, Sprague-DawleyReceptors, Cell SurfaceThalamusConceptsTraumatic brain injurySmall proline-rich repeat protein 1ANogo-66 receptorBrain injuryIpsilateral cortexReticular thalamusNeuN cellsLateral fluid percussion brain injuryTraumatic central nervous system injuryFluid percussion brain injuryAxonal outgrowthCentral nervous system injuryIpsilateral external capsuleOligodendrocyte marker RIPNeuN-positive cellsNeuronal marker NeuNExpression of NogoNervous system injuryWhite matter tractsImportant brain regionsNgR expressionPoor regenerative capacitySPRR1A expressionWestern blot analysisSystem injury