2009
Cellular 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
2006
Subcutaneous Nogo Receptor Removes Brain Amyloid-β and Improves Spatial Memory in Alzheimer's Transgenic Mice
Park JH, Widi GA, Gimbel DA, Harel NY, Lee DH, Strittmatter SM. Subcutaneous Nogo Receptor Removes Brain Amyloid-β and Improves Spatial Memory in Alzheimer's Transgenic Mice. Journal Of Neuroscience 2006, 26: 13279-13286. PMID: 17182778, PMCID: PMC2856604, DOI: 10.1523/jneurosci.4504-06.2006.Peer-Reviewed Original ResearchConceptsAmyloid precursor proteinTransgenic miceAlzheimer's diseaseAbeta clearanceAbeta plaque loadAlzheimer's transgenic miceImproved spatial memoryRadial arm water mazeNogo-66 receptorEffective therapeutic approachPotential therapeutic benefitSpatial memoryAmyloid-beta peptidePlaque loadAbeta levelsBrain amyloidDisease onsetAbeta productionTherapeutic approachesNogo receptorTherapeutic benefitWater mazeInverse correlationAbetaMice