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 ResearchConceptsSynapse 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 ageLongitudinal simultaneous fMRI and mesoscale calcium imaging in a mouse model of Alzheimer’s disease
Mandino F, Shen X, Desrosiers-Gregoire G, O'Connor D, Mukherjee B, DeLuca K, Hamodi A, Owens A, Ha Y, Qu A, Onofrey J, Papademetris X, Chakravarty M, Crair M, Strittmatter S, Lake E. Longitudinal simultaneous fMRI and mesoscale calcium imaging in a mouse model of Alzheimer’s disease. Proceedings Of The International Society For Magnetic Resonance In Medicine ... Scientific Meeting And Exhibition. 2023 DOI: 10.58530/2023/3914.Peer-Reviewed Original ResearchMouse model of Alzheimer's diseaseModel of Alzheimer's diseaseMesoscale calcium imagingAlzheimer's diseaseBehavioral deficitsExcitatory neural activityMultimodal neuroimagingBOLD signalSimultaneous fMRINeuroimaging changesNeural activityBOLD fMRIPreliminary evidenceCalcium imagingClinically accessible biomarkersMesoscopic calcium imagingSpontaneous activityFMRINeuroimagingBOLDDeficitsComplex relationship
2017
Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease
Salazar SV, Gallardo C, Kaufman AC, Herber CS, Haas LT, Robinson S, Manson JC, Lee MK, Strittmatter SM. Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease. Journal Of Neuroscience 2017, 37: 9207-9221. PMID: 28842420, PMCID: PMC5607466, DOI: 10.1523/jneurosci.0722-17.2017.Peer-Reviewed Original ResearchConceptsDisease onsetAlzheimer's diseaseFamilial Alzheimer's diseaseDisease pathophysiologyCellular prion proteinHippocampal synapse lossSoluble oligomeric amyloidTransgenic Alzheimer's diseaseTime of diagnosisDisease-modifying therapiesAlzheimer's disease pathophysiologyPotential therapeutic targetAD-related phenotypesMonths of ageRole of PrPSymptom onsetSynaptic deficitsPrion proteinSynapse lossCatecholaminergic neuronsPlaque densityBehavioral deficitsOligomeric amyloidMouse modelPresent symptoms
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