2012
Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons
Um JW, Nygaard HB, Heiss JK, Kostylev MA, Stagi M, Vortmeyer A, Wisniewski T, Gunther EC, Strittmatter SM. Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons. Nature Neuroscience 2012, 15: 1227-1235. PMID: 22820466, PMCID: PMC3431439, DOI: 10.1038/nn.3178.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBlotting, WesternCalcium SignalingCell LineDendritic SpinesElectroencephalographyEnzyme ActivationHumansMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeuronsPhosphorylationProtein BindingProto-Oncogene Proteins c-fynPrPC ProteinsRatsReceptors, N-Methyl-D-AspartateSeizuresSynapses
2010
Anti-PrPC monoclonal antibody infusion as a novel treatment for cognitive deficits in an alzheimer's disease model mouse
Chung E, Ji Y, Sun Y, Kascsak RJ, Kascsak RB, Mehta PD, Strittmatter SM, Wisniewski T. Anti-PrPC monoclonal antibody infusion as a novel treatment for cognitive deficits in an alzheimer's disease model mouse. BMC Neuroscience 2010, 11: 130. PMID: 20946660, PMCID: PMC2964735, DOI: 10.1186/1471-2202-11-130.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalBlotting, WesternCerebral CortexCognition DisordersEnzyme-Linked Immunosorbent AssayHippocampusHumansImage Processing, Computer-AssistedImmunohistochemistryMemory, Short-TermMiceMice, TransgenicPrPC ProteinsPsychomotor PerformanceSynapsesSynaptophysinConceptsAPP/PS1 Tg miceAPP/PS1 transgenic miceAPP/PS1 TgPS1 transgenic miceDisease model miceTransgenic miceCognitive deficitsTg miceAβ oligomersBehavioral testingVehicle solutionAlzheimer's disease model miceDentate gyrus molecular layerAPP/PS1 groupWild-type control groupConformational neurodegenerative disordersMonoclonal antibody infusionAD transgenic miceAmyloid plaque burdenAβ oligomer levelsDays/weekNovel therapeutic approachesMurine hippocampal slicesShort-term treatmentAnti-PrP antibodies
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