2023
TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury
Shafit-Zagardo B, Sidoli S, Goldman J, DuBois J, Corboy J, Strittmatter S, Guzik H, Edema U, Arackal A, Botbol Y, Merheb E, Nagra R, Graff S. TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury. Cells 2023, 12: 1734. PMID: 37443768, PMCID: PMC10340176, DOI: 10.3390/cells12131734.Peer-Reviewed Original ResearchConceptsAxonal damageMultiple sclerosisRelapsing-remitting multiple sclerosisHypomorphic miceExperimental autoimmune encephalomyelitisRelapsing-remitting MSNormal-appearing white matterMultiple sclerosis plaquesWhite matter plaquesNon-neurologic controlsWild-type miceBrains of individualsLipid droplet accumulationAutoimmune encephalomyelitisMyelin oligodendrocyteCNS injuryLipid clearanceSpinal cordNeuronal integrityTransmembrane protein 106BWhite matterAlzheimer's diseaseMice resultsDroplet accumulationPlaques
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 basisPathogenesisDementiaProteinPlaquesImpairment
2009
β-amyloid oligomers and cellular prion protein in Alzheimer’s disease
Gunther EC, Strittmatter SM. β-amyloid oligomers and cellular prion protein in Alzheimer’s disease. Journal Of Molecular Medicine 2009, 88: 331-338. PMID: 19960174, PMCID: PMC2846635, DOI: 10.1007/s00109-009-0568-7.Peer-Reviewed Original ResearchConceptsCreutzfeldt-Jakob diseaseAβ oligomersDisease pathophysiologyCellular prion proteinProgression of ADAlzheimer's disease pathophysiologyΒ-amyloid oligomersΒ-amyloid peptidePrion proteinBrain slicesAlzheimer's diseaseSynaptic functionFunctional receptorsNeurodegenerative diseasesDiseasePotential mediatorsAβ assembliesReceptorsAβ monomersPrPCPathophysiologyNeurotoxicityPlaquesProgressionCellular Prion Protein Mediates the Toxicity of β-Amyloid Oligomers: Implications for Alzheimer Disease
Nygaard HB, Strittmatter SM. Cellular Prion Protein Mediates the Toxicity of β-Amyloid Oligomers: Implications for Alzheimer Disease. JAMA Neurology 2009, 66: 1325-1328. PMID: 19901162, PMCID: PMC2849161, DOI: 10.1001/archneurol.2009.223.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseCellular prion proteinPathogenesis of ADBeta-amyloid plaquesAge-related dementiaSoluble oligomeric assembliesPrion proteinPotential clinical implicationsBeta-amyloid oligomersΒ-amyloid oligomersHigh-affinity receptorCommon causeSynaptic plasticityTherapeutic interventionsClinical implicationsAbeta oligomersNovel targetRecent evidenceToxic effectsDiseasePathogenesisDementiaAbetaPlaquesBrain