Featured Publications
TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy
Yuan P, Condello C, Keene CD, Wang Y, Bird TD, Paul SM, Luo W, Colonna M, Baddeley D, Grutzendler J. TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy. Neuron 2016, 90: 724-739. PMID: 27196974, PMCID: PMC4898967, DOI: 10.1016/j.neuron.2016.05.003.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseAxonal dystrophyAmyloid depositsAD-like miceHuman AD tissueLate-onset Alzheimer's diseaseNovel therapeutic strategiesTREM2 deficiencyTau hyperphosphorylationAD tissueMicroglia processesPharmacological modulationCompact plaquesTherapeutic strategiesHigh-resolution confocalTREM2 mutationsTREM2Barrier functionMiceGreater surface exposureAmyloid fibrilsHaplodeficiencyPlaquesDiseaseDystrophy
2007
Various Dendritic Abnormalities Are Associated with Fibrillar Amyloid Deposits in Alzheimer's Disease
GRUTZENDLER J, HELMIN K, TSAI J, GAN W. Various Dendritic Abnormalities Are Associated with Fibrillar Amyloid Deposits in Alzheimer's Disease. Annals Of The New York Academy Of Sciences 2007, 1097: 30-39. PMID: 17413007, DOI: 10.1196/annals.1379.003.Peer-Reviewed Original ResearchConceptsAmyloid depositsAlzheimer's diseasePSAPP miceFibrillar amyloid depositsAmyloid depositionDendritic abnormalitiesHuman AD tissueFibrillar amyloid depositionHuman AD brainsTransgenic mouse modelHuman postmortem brainDystrophic neuritesSpine lossAD brainAD tissueAmyloid plaquesCommon abnormalityMouse modelPostmortem brainsDendritic spinesNeuronal circuitsVaricosity formationSynaptic structureDiseaseDendritic branches