2023
Neuronal transcriptome, tau and synapse loss in Alzheimer’s knock-in mice require prion protein
Stoner A, Fu L, Nicholson L, Zheng C, Toyonaga T, Spurrier J, Laird W, Cai Z, Strittmatter S. Neuronal transcriptome, tau and synapse loss in Alzheimer’s knock-in mice require prion protein. Alzheimer's Research & Therapy 2023, 15: 201. PMID: 37968719, PMCID: PMC10647125, DOI: 10.1186/s13195-023-01345-z.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalMiceMice, TransgenicNeuronsPrion ProteinsPrionsSynapsesTau ProteinsTranscriptomeConceptsSynapse lossDKI miceTau accumulationBrain immune activationNeural network dysfunctionPhospho-tau accumulationAccumulation of tauNeuronal genesInflammatory markersAD miceAβ levelsPrion proteinDystrophic neuritesImmune activationTau pathologyNeuronal gene expressionAmyloid-β OligomersGliotic reactionNetwork dysfunctionBehavioral deficitsSynaptic failureAD modelMemory impairmentAlzheimer's diseaseFunction of age
2022
Reversal of synapse loss in Alzheimer mouse models by targeting mGluR5 to prevent synaptic tagging by C1Q
Spurrier J, Nicholson L, Fang XT, Stoner AJ, Toyonaga T, Holden D, Siegert TR, Laird W, Allnutt MA, Chiasseu M, Brody AH, Takahashi H, Nies SH, Pérez-Cañamás A, Sadasivam P, Lee S, Li S, Zhang L, Huang YH, Carson RE, Cai Z, Strittmatter SM. Reversal of synapse loss in Alzheimer mouse models by targeting mGluR5 to prevent synaptic tagging by C1Q. Science Translational Medicine 2022, 14: eabi8593. PMID: 35648810, PMCID: PMC9554345, DOI: 10.1126/scitranslmed.abi8593.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAnimalsComplement C1qDisease Models, AnimalMiceReceptor, Metabotropic Glutamate 5SynapsesConceptsPositron emission tomographySilent allosteric modulatorsAlzheimer's diseaseMouse modelPhospho-tau accumulationAged mouse modelAlzheimer mouse modelImmune-mediated attackSAM treatmentMicroglial mediatorsSynaptic engulfmentSynaptic lossAD miceComplement component C1qSynapse lossGlutamate responseSynaptic densityDrug washoutSynaptic localizationTherapeutic benefitCognitive impairmentAllosteric modulatorsEmission tomographyNonhuman primatesComponent C1q
2012
Dependence of Regenerated Sensory Axons on Continuous Neurotrophin-3 Delivery
Hou S, Nicholson L, van Niekerk E, Motsch M, Blesch A. Dependence of Regenerated Sensory Axons on Continuous Neurotrophin-3 Delivery. Journal Of Neuroscience 2012, 32: 13206-13220. PMID: 22993437, PMCID: PMC3513675, DOI: 10.1523/jneurosci.5041-11.2012.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAntigensAxonsCell TransplantationCells, CulturedCholera ToxinDisease Models, AnimalDoxycyclineEnzyme-Linked Immunosorbent AssayFemaleGene Expression RegulationGenetic TherapyGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsHEK293 CellsHumansLamininLeukocyte L1 Antigen ComplexMembrane GlycoproteinsMicrotubule-Associated ProteinsMyelin-Oligodendrocyte GlycoproteinNerve Growth FactorsNerve RegenerationNerve Tissue ProteinsNeurofilament ProteinsNeurotrophin 3ProteoglycansRatsRats, Inbred F344S100 Calcium Binding Protein beta SubunitS100 ProteinsSchwann CellsSciatic NerveSensory Receptor CellsSpinal Cord InjuriesStem Cell TransplantationTime FactorsTransfectionConceptsNT-3 expressionRegenerated sensory axonsRegenerated axonsSensory axonsLesion siteNeurotrophin-3Dorsal column sensory axonsLesion/graft siteNT-3 gene expressionSpinal cord lesion siteCholera toxin βNT-3 deliveryIntrinsic growth capacityBone marrow stromal cellsAxodendritic synapsesConditioning lesionPresynaptic markersAxon numberSpinal cordMarrow stromal cellsSchwann cellsSensory neuronsAdult ratsDoxycycline administrationGraft site