2022
PET Imaging of Synaptic Density: Challenges and Opportunities of Synaptic Vesicle Glycoprotein 2A PET in Small Animal Imaging
Toyonaga T, Fesharaki-Zadeh A, Strittmatter SM, Carson RE, Cai Z. PET Imaging of Synaptic Density: Challenges and Opportunities of Synaptic Vesicle Glycoprotein 2A PET in Small Animal Imaging. Frontiers In Neuroscience 2022, 16: 787404. PMID: 35345546, PMCID: PMC8957200, DOI: 10.3389/fnins.2022.787404.Peer-Reviewed Original ResearchAnimal modelsPET imaging studiesPET imagingImaging studiesSynaptic vesicle glycoprotein 2ADisease animal modelsOngoing clinical investigationsDifferent injection routesSynaptic densityClinical investigationPharmacological effectsRodent brainNovel interventionsInjection routeNeurodegenerative disordersNeuropsychiatric diseasesPET studiesBrainMultiple diseasesPET centersDiseaseInjectable volumeImagingSmaller brainsPET
2011
Cartilage Acidic Protein–1B (LOTUS), an Endogenous Nogo Receptor Antagonist for Axon Tract Formation
Sato Y, Iketani M, Kurihara Y, Yamaguchi M, Yamashita N, Nakamura F, Arie Y, Kawasaki T, Hirata T, Abe T, Kiyonari H, Strittmatter SM, Goshima Y, Takei K. Cartilage Acidic Protein–1B (LOTUS), an Endogenous Nogo Receptor Antagonist for Axon Tract Formation. Science 2011, 333: 769-773. PMID: 21817055, PMCID: PMC3244695, DOI: 10.1126/science.1204144.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBinding SitesCalcium-Binding ProteinsCell LineCells, CulturedGPI-Linked ProteinsGrowth ConesHumansImmunohistochemistryLigandsMiceMice, Inbred ICRMyelin ProteinsNogo ProteinsNogo Receptor 1Olfactory PathwaysProsencephalonProtein BindingReceptors, Cell SurfaceSignal TransductionConceptsTract formationNogo receptor 1Axon growth inhibitorsProtein 1BEndogenous antagonismAxon tract formationReceptor antagonistGrowth cone collapseAxonal projectionsCircuitry formationNeural circuitry formationMouse brainReceptor 1LOT formationNeural regenerationNgR1Key moleculesCone collapseMiceFluorophore-assisted light inactivationGrowth inhibitorAntagonistBrainMyelinNogo
2010
Lynx for Braking Plasticity
Higley MJ, Strittmatter SM. Lynx for Braking Plasticity. Science 2010, 330: 1189-1190. PMID: 21109660, PMCID: PMC3244692, DOI: 10.1126/science.1198983.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAgingAmblyopiaAnimalsChondroitin Sulfate ProteoglycansDominance, OcularMembrane GlycoproteinsMiceMice, KnockoutNeuronal PlasticityNeuropeptidesNicotinic AntagonistsReceptors, ImmunologicReceptors, NicotinicSensory DeprivationSignal TransductionVision, OcularVisual CortexVisual PathwaysConceptsVisual cortex plasticityVisual cortex neuronsNicotinic acetylcholine receptorsJuvenile plasticityNeurological performanceCortex neuronsJuvenile brainOcular dominanceAdult miceAcetylcholine receptorsVisual cortexAdult animalsSensory inputAdultsYoung mammalsMiceMedical implicationsEyesSuch plasticityPlasticityCortexNeuronsBrainReceptorsSortilin-Mediated Endocytosis Determines Levels of the Frontotemporal Dementia Protein, Progranulin
Hu F, Padukkavidana T, Vægter CB, Brady OA, Zheng Y, Mackenzie IR, Feldman HH, Nykjaer A, Strittmatter SM. Sortilin-Mediated Endocytosis Determines Levels of the Frontotemporal Dementia Protein, Progranulin. Neuron 2010, 68: 654-667. PMID: 21092856, PMCID: PMC2990962, DOI: 10.1016/j.neuron.2010.09.034.Peer-Reviewed Original ResearchConceptsFrontotemporal lobar degenerationSerum PGRN levelsFTLD-TDP casesFTLD-TDPMicroglial cellsPGRN levelsCortical neuronsGRN haploinsufficiencyProgranulin mutationsTDP-43Causative rolePGRNUbiquitin aggregatesNeuronsSortilinMiceCell surfaceDetermine levelsPathophysiologyInjuryProgranulinCNSCentral roleDegenerationBrain
2009
Cellular Prion Protein Mediates the Toxicity of β-Amyloid Oligomers: Implications for Alzheimer Disease
Nygaard HB, Strittmatter SM. Cellular Prion Protein Mediates the Toxicity of β-Amyloid Oligomers: Implications for Alzheimer Disease. JAMA Neurology 2009, 66: 1325-1328. PMID: 19901162, PMCID: PMC2849161, DOI: 10.1001/archneurol.2009.223.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseCellular prion proteinPathogenesis of ADBeta-amyloid plaquesAge-related dementiaSoluble oligomeric assembliesPrion proteinPotential clinical implicationsBeta-amyloid oligomersΒ-amyloid oligomersHigh-affinity receptorCommon causeSynaptic plasticityTherapeutic interventionsClinical implicationsAbeta oligomersNovel targetRecent evidenceToxic effectsDiseasePathogenesisDementiaAbetaPlaquesBrain
2008
Axonal growth therapeutics: regeneration or sprouting or plasticity?
Cafferty WB, McGee AW, Strittmatter SM. Axonal growth therapeutics: regeneration or sprouting or plasticity? Trends In Neurosciences 2008, 31: 215-220. PMID: 18395807, PMCID: PMC2678051, DOI: 10.1016/j.tins.2008.02.004.Peer-Reviewed Original ResearchConceptsAxonal growthAstroglial scarHigh clinical significanceFunctional recoveryNeurological injuryInciting eventFunctional deficitsSpinal cordClinical significanceAdult brainLoss of functionCell lossInhibitory factorAxonal connectivityAxonal anatomyAxonal extensionMolecular interventionsMyelinScarCordInjuryBrain
2006
Axonal Regeneration and Recovery From Chronic Central Nervous System Injury
Strittmatter S. Axonal Regeneration and Recovery From Chronic Central Nervous System Injury. 2006, 1165-1172. DOI: 10.1007/978-1-59259-963-9_122.Peer-Reviewed Original ResearchAxonal regenerationChronic central nervous system injuryCentral nervous system injuryNervous system injuryChronic neurological dysfunctionRecovery of functionTreatment of dysfunctionSystem injuryPersistent dysfunctionNeurological dysfunctionSpinal cordNeurological conditionsAdult brainTrophic factorsNeuronal connectivityDysfunctionNeuronsRecent scientific advancesStem cellsCellsTransplantationCordInjuryBrainRecovery
1986
Parkinson's disease: Nigral receptor changes support peptidergic role in nigrostriatal modulation
Uhl G, Hackney G, Torchia M, Stranov V, Tourtellotte W, Whitehouse P, Tran V, Strittmatter S. Parkinson's disease: Nigral receptor changes support peptidergic role in nigrostriatal modulation. Annals Of Neurology 1986, 20: 194-203. PMID: 3019228, DOI: 10.1002/ana.410200204.Peer-Reviewed Original ResearchConceptsKappa-opiate receptorsIdiopathic Parkinson's diseaseNormal human brainNigrostriatal circuitryPeptidergic influencesReceptor changesSubstantia nigraMore modest reductionsSerotonin receptorsParkinson's diseaseBenzodiazepine receptorsAutoradiographic studyModest reductionReceptorsAngiotensinSomatostatinHuman brainDiseaseDopamineBenzodiazepines IPatientsNeurotensinSubtypesBrainNigra
1985
Substance K and substance P as possible endogenous substrates of angiotensin converting enzyme in the brain
Thiele E, Strittmatter S, Snyder S. Substance K and substance P as possible endogenous substrates of angiotensin converting enzyme in the brain. Biochemical And Biophysical Research Communications 1985, 128: 317-324. PMID: 2580530, DOI: 10.1016/0006-291x(85)91681-x.Peer-Reviewed Original Research