2023
Prion Protein Complex with mGluR5 Mediates Amyloid-ß Synaptic Loss in Alzheimer’s Disease
Roseman G, Fu L, Strittmatter S. Prion Protein Complex with mGluR5 Mediates Amyloid-ß Synaptic Loss in Alzheimer’s Disease. 2023, 467-481. DOI: 10.1007/978-3-031-20565-1_22.ChaptersAlzheimer's diseaseMouse modelAD transgenic mouse modelLong-term potentiation impairmentPrimary histopathological featureAD mouse modelAmyloid-beta plaquesTransgenic mouse modelPotential therapeutic targetSynaptic lossHistopathological featuresAD pathophysiologyNeuronal dysfunctionSynapse densityCognitive dysfunctionNeurofibrillary tanglesTherapeutic targetMemory deficitsCellular prion proteinMGluR5DiseaseCell death characteristicCommon formSynaptotoxicityDysfunction
2017
Chapter Thirteen Synaptotoxic Signaling by Amyloid Beta Oligomers in Alzheimer's Disease Through Prion Protein and mGluR5
Brody AH, Strittmatter SM. Chapter Thirteen Synaptotoxic Signaling by Amyloid Beta Oligomers in Alzheimer's Disease Through Prion Protein and mGluR5. Advances In Pharmacology 2017, 82: 293-323. PMID: 29413525, PMCID: PMC5835229, DOI: 10.1016/bs.apha.2017.09.007.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseNovel potential therapeutic targetDisease-modifying AD therapiesPotential therapeutic targetAmyloid-beta oligomersPrion proteinSynapse lossTau pathologySynaptic dysfunctionAD symptomsSynaptic damageAD pathophysiologyNeuronal dysfunctionSynaptic toxicityDisease progressionAD progressionAD therapyMemory dysfunctionTherapeutic targetCellular prion proteinBeta oligomersDysfunctionDiseaseGlobal health crisisMGluR5Conditional 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