2017
Opposing effects of progranulin deficiency on amyloid and tau pathologies via microglial TYROBP network
Takahashi H, Klein ZA, Bhagat SM, Kaufman AC, Kostylev MA, Ikezu T, Strittmatter SM, For the Alzheimer’s Disease Neuroimaging Initiative. Opposing effects of progranulin deficiency on amyloid and tau pathologies via microglial TYROBP network. Acta Neuropathologica 2017, 133: 785-807. PMID: 28070672, PMCID: PMC5391267, DOI: 10.1007/s00401-017-1668-z.Peer-Reviewed Original ResearchConceptsAPP/PS1 micePS1 micePGRN deficiencyAlzheimer's diseaseAD risk variantsCerebrospinal fluid Aβ levelsLoss of progranulinMicroglial Aβ phagocytosisCSF tau levelsFrontotemporal lobar degenerationRisk variantsAPPswe/Aβ phagocytosisNeuronal injuryAβ levelsAβ pathologyCerebral amyloidosisAxonal dystrophyTau pathologyTau levelsComplement depositionPGRN levelsAD pathophysiologyAmyloid imagingProgranulin deficiency
2016
Binding Sites for Amyloid-β Oligomers and Synaptic Toxicity
Smith LM, Strittmatter SM. Binding Sites for Amyloid-β Oligomers and Synaptic Toxicity. Cold Spring Harbor Perspectives In Medicine 2016, 7: a024075. PMID: 27940601, PMCID: PMC5411685, DOI: 10.1101/cshperspect.a024075.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseAβ oligomersSoluble Aβ oligomersFibrillary amyloidNeuronal impairmentSynaptic dysfunctionAD pathogenesisSynaptic toxicityAmyloid-β OligomersCellular prion proteinNeuronal cascadesFurther studiesCell surface proteinsDiseaseAβPrion proteinOligomer toxicityToxicityDysfunctionMolecular basisPathogenesisDementiaProteinPlaquesImpairmentEarly Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease.
Heiss JK, Barrett J, Yu Z, Haas LT, Kostylev MA, Strittmatter SM. Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease. Cerebral Cortex 2016, 27: 3660-3674. PMID: 27365298, PMCID: PMC6059166, DOI: 10.1093/cercor/bhw188.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsCerebral CortexDendritic SpinesDisease Models, AnimalGene Expression ProfilingGreen Fluorescent ProteinsHippocampusHumansImaging, Three-DimensionalImmunoprecipitationMiceMice, Inbred C57BLMice, TransgenicMutationNeuroimagingPlaque, AmyloidPresenilin-1Prion ProteinsProto-Oncogene Proteins c-fosSensory DeprivationTime FactorsVibrissaeConceptsAPP/PS1 miceDendritic spine turnoverSpine turnoverAlzheimer's diseasePS1 miceAged APP/PS1 miceYoung APP/PS1 miceAPP/PS1 mouse brainSoluble Aβ oligomersLipid-metabolizing genesAPPswe/Synaptic lossCerebral cortexSynapse densityAβ plaquesSynaptic dysregulationLack responsivenessMouse modelDendritic spinesPersistent spinesSynapse turnoverPlaque formationMouse brainYounger ageCellular prion protein
2013
Delayed amyloid plaque deposition and behavioral deficits in outcrossed AβPP/PS1 mice
Couch BA, Kerrisk ME, Kaufman AC, Nygaard HB, Strittmatter SM, Koleske AJ. Delayed amyloid plaque deposition and behavioral deficits in outcrossed AβPP/PS1 mice. The Journal Of Comparative Neurology 2013, 521: 1395-1408. PMID: 23047754, PMCID: PMC3562562, DOI: 10.1002/cne.23239.Peer-Reviewed Original ResearchConceptsAβPP/PS1 micePS1 micePlaque burdenPlaque depositionBehavioral deficitsRadial arm water maze performanceBehavioral impairmentsAlzheimer's diseaseAβPP processingPresenilin 1Amyloid-β precursor proteinLower plaque burdenProgressive neurodegenerative dementiaAmyloid plaque depositionAmyloid plaque accumulationAmyloid plaque burdenAD-like featuresNovel object recognitionWater maze performanceMonths of ageDendrite lossAD progressionNeurodegenerative dementiaPlaque accumulationMixed genetic background
2006
Alzheimer Precursor Protein Interaction with the Nogo-66 Receptor Reduces Amyloid-β Plaque Deposition
Park JH, Gimbel DA, GrandPre T, Lee JK, Kim JE, Li W, Lee DH, Strittmatter SM. Alzheimer Precursor Protein Interaction with the Nogo-66 Receptor Reduces Amyloid-β Plaque Deposition. Journal Of Neuroscience 2006, 26: 1386-1395. PMID: 16452662, PMCID: PMC2846286, DOI: 10.1523/jneurosci.3291-05.2006.Peer-Reviewed Original ResearchConceptsAmyloid precursor proteinAlzheimer's diseaseAbeta levelsDystrophic neuritesPlaque depositionAmyloid-β plaque depositionCourse of ADAbeta plaque depositionTransgenic AD modelBrain Abeta levelsAD brain samplesAdult CNS axonsAxonal sprouting responseNgR expressionAbeta depositsAxonal dysfunctionPathophysiologic hypothesesSecretase processingTraumatic injuryAbeta productionDisease processAD modelBrain samplesCNS axonsPlaque deposits