2022
TREM2 Deficiency Disrupts Network Oscillations Leading to Epileptic Activity and Aggravates Amyloid-β-Related Hippocampal Pathophysiology in Mice
Stoiljkovic M, Gutierrez KO, Kelley C, Horvath TL, Hajós M. TREM2 Deficiency Disrupts Network Oscillations Leading to Epileptic Activity and Aggravates Amyloid-β-Related Hippocampal Pathophysiology in Mice. Journal Of Alzheimer’s Disease 2022, 88: 837-847. PMID: 34120899, PMCID: PMC8898080, DOI: 10.3233/jad-210041.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseMicroglial functionTREM2 functionTheta-phase gamma-amplitude couplingHippocampal network functionSpontaneous epileptiform seizuresNetwork oscillationsTransgenic AD modelHippocampal neuronal excitabilityMyeloid cells 2Clinical Alzheimer's diseaseWild-type miceHippocampal network oscillationsHippocampal pathophysiologyProgressive dementiaTau pathologyUrethane anesthesiaAD pathophysiologyNeuronal excitabilityEpileptiform seizuresEpileptic activityAD modelTREM2Disease pathologyCells 2Impact of TREM2 on hippocampal network oscillations in Tg2576 mice modeling amyloid‐β pathology
Stoiljkovic M, Gutierrez K, Kelley C, Horvath T, Hajos M. Impact of TREM2 on hippocampal network oscillations in Tg2576 mice modeling amyloid‐β pathology. Alzheimer's & Dementia 2022, 17 DOI: 10.1002/alz.054379.Peer-Reviewed Original ResearchAlzheimer's diseaseNeuronal network oscillationsMicroglial functionNetwork oscillationsStimulation-induced hippocampal theta oscillationTheta-phase gamma-amplitude couplingImpact of TREM2Spontaneous epileptiform seizuresTransgenic AD modelMyeloid cells 2Wild-type miceHippocampal network oscillationsHippocampal theta oscillationsProgressive dementiaTau pathologyUrethane anesthesiaLocal field potentialsCA1 regionFunctional impairmentAβ overproductionEpileptiform seizuresAD modelTREM2Phase-amplitude couplingDisease pathology
2010
Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein
Gimbel DA, Nygaard HB, Coffey EE, Gunther EC, Laurén J, Gimbel ZA, Strittmatter SM. Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein. Journal Of Neuroscience 2010, 30: 6367-6374. PMID: 20445063, PMCID: PMC3323924, DOI: 10.1523/jneurosci.0395-10.2010.Peer-Reviewed Original ResearchConceptsTransgenic miceAlzheimer's diseaseCellular prion proteinSpatial learningAD transgenic miceTransgenic AD modelTransgenic Alzheimer's micePrnp-/- miceAD-related phenotypesAmyloid-beta peptideAbeta accumulationAbeta plaquesAbeta levelsAD micePrion proteinAlzheimer's miceAxonal degenerationAPP expressionSynaptic markersHippocampal slicesDetectable impairmentEarly deathAD modelBehavioral impairmentsMemory impairment
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
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