2019
Mechanisms of hyperexcitability in Alzheimer’s disease hiPSC-derived neurons and cerebral organoids vs isogenic controls
Ghatak S, Dolatabadi N, Trudler D, Zhang X, Wu Y, Mohata M, Ambasudhan R, Talantova M, Lipton S. Mechanisms of hyperexcitability in Alzheimer’s disease hiPSC-derived neurons and cerebral organoids vs isogenic controls. ELife 2019, 8: e50333. PMID: 31782729, PMCID: PMC6905854, DOI: 10.7554/elife.50333.Peer-Reviewed Original ResearchConceptsDisease brainNeuronal culturesHuman Alzheimer's disease brainCerebral organoidsAD-related mutationsHiPSC-derived neuronsTransgenic AD miceInhibitory synaptic activityMechanisms of hyperexcitabilityAlzheimer's disease brainAberrant electrical activitySodium current densityAD micePathophysiological correlatesSynaptic dysfunctionAD pathophysiologyExcessive excitabilitySynaptic activityObserved hyperexcitabilityCognitive declineBursting activityHyperexcitabilityPresenilin 1Electrical activityNeurite length
2013
Growth Factor Receptor-Bound Protein 2 Promotes Autophagic Removal of Amyloid-β Protein Precursor Intracellular Domain Overload in Neuronal Cells
Roy K, Raychaudhuri M, Chakrabarti O, Mukhopadhyay D. Growth Factor Receptor-Bound Protein 2 Promotes Autophagic Removal of Amyloid-β Protein Precursor Intracellular Domain Overload in Neuronal Cells. Journal Of Alzheimer’s Disease 2013, 38: 881-895. PMID: 24100123, DOI: 10.3233/jad-130929.Peer-Reviewed Original ResearchConceptsAmyloid-β protein precursor intracellular domainRole of Grb2Dynamin-independent mannerTypes of vesiclesAutophagic removalApoptosis pointsGrowth factor receptorIntracellular domainVesicle accumulationCaspase activityDisease brainNeuronal cellsAD cell modelGrb2Independent mannerFactor receptorVesiclesAutophagosomesExcess conditionsAlzheimer's disease brainProtein overloadStudy unravelsCell modelCytotoxic effectsCells
2012
Association of COL25A1 with Comorbid Antisocial Personality Disorder and Substance Dependence
Li D, Zhao H, Kranzler HR, Oslin D, Anton RF, Farrer LA, Gelernter J. Association of COL25A1 with Comorbid Antisocial Personality Disorder and Substance Dependence. Biological Psychiatry 2012, 71: 733-740. PMID: 22297151, PMCID: PMC3548659, DOI: 10.1016/j.biopsych.2011.12.011.Peer-Reviewed Original ResearchConceptsSingle nucleotide polymorphismsTwo-stage genetic association studyType II transmembrane proteinCase-control cohortAllelic p-valueAlpha 1 geneSame single nucleotide polymorphismIndependent case-control cohortsTransmembrane proteinTranscription factorsSNP mapGenetic association studiesEuropean American casesCandidate genesCOL25A1 geneAssociation studiesGenetic studiesFamily-based cohortChromosome 4q25GenesNucleotide polymorphismsCOL25A1Alzheimer's disease brainLong-term patternsDiscovery stage
2008
p21-activated Kinase-aberrant Activation and Translocation in Alzheimer Disease Pathogenesis*
Ma QL, Yang F, Calon F, Ubeda OJ, Hansen JE, Weisbart RH, Beech W, Frautschy SA, Cole GM. p21-activated Kinase-aberrant Activation and Translocation in Alzheimer Disease Pathogenesis*. Journal Of Biological Chemistry 2008, 283: 14132-14143. PMID: 18347024, PMCID: PMC2376243, DOI: 10.1074/jbc.m708034200.Peer-Reviewed Original ResearchConceptsCultured hippocampal neuronsAlzheimer's diseaseHippocampal neuronsDendritic spinesTransgenic miceAlzheimer's disease brainAlzheimer's amyloid pathologyAlzheimer's disease (AD) pathogenesisBeta-amyloid oligomersOligomer treatmentSrc family tyrosine kinase inhibitor PP2P-NR2BSynaptic deficitsAmyloid pathologyDisease brainTyrosine kinase inhibitor PP2Disease pathogenesisCognitive deficitsMental retardation syndromeProtein drebrinKinase inhibitor PP2DiseaseNeuronsRetardation syndromeMice
2000
Amyloid Beta-Induced Neuronal Death is Bax-Dependent but Caspase-Independent
Selznick L, Zheng T, Flavell R, Rakic P, Roth K. Amyloid Beta-Induced Neuronal Death is Bax-Dependent but Caspase-Independent. Journal Of Neuropathology & Experimental Neurology 2000, 59: 271-279. PMID: 10759182, DOI: 10.1093/jnen/59.4.271.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid Chloromethyl KetonesAmyloid beta-PeptidesAnimalsApoptosisbcl-2-Associated X ProteinCaspase 3Caspase InhibitorsCaspasesCell DeathCells, CulturedCysteine Proteinase InhibitorsDose-Response Relationship, DrugFemaleGlycoproteinsIn Situ Nick-End LabelingMaleMiceMice, KnockoutMicrotubule-Associated ProteinsMicrotubulesNeuronsPaclitaxelProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2TelencephalonConceptsNeuronal deathNeuronal apoptosisCaspase-3 activationTelencephalic neuronsFibrillar amyloid-beta (Abeta) peptidesAbeta-induced neuronal apoptosisAD treatment strategiesAbeta-induced neuronal deathPathogenesis of ADAlzheimer's disease brainEffects of AbetaAmyloid-beta peptideApoptotic nuclear featuresUnderlying pathophysiologyTreatment strategiesDisease brainSenile plaquesNeurotoxic effectsAmyloid betaCalpain inhibitionPharmacological inhibitionBeta peptideNuclear featuresAbetaCaspase-3
1996
Glycation and microglial reaction in lesions of Alzheimer's disease
Dickson D, Sinicropi S, Yen S, Ko L, Mattiace L, Bucala R, Vlassara H. Glycation and microglial reaction in lesions of Alzheimer's disease. Neurobiology Of Aging 1996, 17: 733-743. PMID: 8892346, DOI: 10.1016/0197-4580(96)00116-9.Peer-Reviewed Original ResearchConceptsAdvanced glycation end productsAGE immunoreactivityNeurofibrillary tanglesExtracellular neurofibrillary tanglesAmyloid depositsMicroglial reactionActivation of microgliaIntracellular neurofibrillary tanglesAlzheimer's disease brainPattern of immunoreactivityGlycation end productsTriple immunostainingDisease brainSenile plaquesDiffuse amyloidAlzheimer's diseaseImmunoreactivityCryostat sectionsDouble labelingAntibodiesMicrogliaLesionsPolyclonal antibodiesDiseaseGlycation
1992
Increased phosphorylation of elongation factor 2 in Alzheimer's disease
Johnson G, Gotlib J, Haroutunian V, Bierer L, Nairn A, Merril C, Wallace W. Increased phosphorylation of elongation factor 2 in Alzheimer's disease. Brain Research 1992, 15: 319-326. PMID: 1331687, DOI: 10.1016/0169-328x(92)90124-t.Peer-Reviewed Original ResearchConceptsDisease brainAlzheimer's diseaseAlzheimer's disease brainFactor 2AD homogenatesAD tissueElongation factor 2Brain homogenatesSame brainDiseaseVariant isoformsProtein synthesisPhosphorylated formInhibits protein synthesisBrainUnaffected areasHomogenatesAcidic isoformsPhosphorylationGene expressionEF-2
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