2025
[18F]MK-6240 Radioligand Delivery Indices as Surrogates of Cerebral Perfusion: Bias and Correlation Against [15O]Water.
Fu J, Juttukonda M, Garimella A, Salvatore A, Lois C, Ranasinghe A, Efthimiou N, Sari H, Aye W, Guehl N, El Fakhri G, Johnson K, Dickerson B, Izquierdo-Garcia D, Catana C, Price J. [18F]MK-6240 Radioligand Delivery Indices as Surrogates of Cerebral Perfusion: Bias and Correlation Against [15O]Water. Journal Of Nuclear Medicine 2025, 66: 410-417. PMID: 39947916, PMCID: PMC11876731, DOI: 10.2967/jnumed.124.268701.Peer-Reviewed Original Research
2024
Plasma Aβ42/Aβ40 is sensitive to early cerebral amyloid accumulation and predicts risk of cognitive decline across the Alzheimer's disease spectrum
Trelle A, Young C, Vossler H, Benitez J, Cody K, Mendiola J, Swarovski M, Le Guen Y, Feinstein I, Butler R, Channappa D, Romero A, Park J, Shahid‐Besanti M, Corso N, Chau K, Smith A, Skylar‐Scott I, Yutsis M, Fredericks C, Tian L, Younes K, Kerchner G, Deutsch G, Davidzon G, Sha S, Henderson V, Longo F, Greicius M, Wyss‐Coray T, Andreasson K, Poston K, Wagner A, Mormino E, Wilson E. Plasma Aβ42/Aβ40 is sensitive to early cerebral amyloid accumulation and predicts risk of cognitive decline across the Alzheimer's disease spectrum. Alzheimer's & Dementia 2024, 21: e14442. PMID: 39713875, PMCID: PMC11848181, DOI: 10.1002/alz.14442.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseCognitive declinePositron emission tomographyAmyloid-betaTau accumulationAmyloid positivityHippocampal-dependent memoryAlzheimer's disease spectrumAmyloidAmyloid accumulationTau burdenAb accumulationRisk of cognitive declineSensitive to memoryTau positron emission tomographyAlzheimer's Disease Research CenterPredicting cognitive declineAlzheimerTauScalable biomarkersAD continuumCerebral amyloid accumulationCross-sectional associationsCI individualsAccumulationTau pathology is associated with synaptic density and longitudinal synaptic loss in Alzheimer’s disease
Wang J, Huang Q, Chen X, You Z, He K, Guo Q, Huang Y, Yang Y, Lin Z, Guo T, Zhao J, Guan Y, Li B, Xie F. Tau pathology is associated with synaptic density and longitudinal synaptic loss in Alzheimer’s disease. Molecular Psychiatry 2024, 29: 2799-2809. PMID: 38589563, DOI: 10.1038/s41380-024-02501-z.Peer-Reviewed Original ResearchTau pathologySynaptic lossTau tanglesAlzheimer's diseaseAssociated with synaptic lossAD patientsMild cognitive impairmentMild cognitive impairment patientsAmyloid-bPlasma p-tauP-tau181 levelsAssociation of ABSynaptic densityP-tauNormal controlsPositron emission tomographyMediation analysisTemporal lobeTauTau burdenP-tau181One-year follow-up assessmentSeventy-five participantsTanglesFollow-up assessmentMulti-modal Neuroimaging Phenotyping of Mnemonic Anosognosia in the Aging Brain
Bueichekú E, Diez I, Gagliardi G, Kim C, Mimmack K, Sepulcre J, Vannini P. Multi-modal Neuroimaging Phenotyping of Mnemonic Anosognosia in the Aging Brain. Communications Medicine 2024, 4: 65. PMID: 38580832, PMCID: PMC10997795, DOI: 10.1038/s43856-024-00497-9.Peer-Reviewed Original ResearchMemory declineMedial anterior prefrontal cortexAging brainWhole-brain voxel-wiseAnterior prefrontal cortexRegion-of-interest analysisResting-state functional MRIObjective memory declineOccipito-parietal regionsMulti-modal neuroimagingNetwork connectivity patternsAlzheimer's diseaseFunctional connectivity networksPrefrontal cortexMnemonic anosognosiaTau burdenBiomarkers of AD pathologyMode networkParieto-occipital areasFunctional network connectivity disruptionFunctional MRIBrain phenotypesVoxel-wiseBehavioral conditionsBehavioral biomarkers
2023
Multi‐modal Neuroimaging Phenotyping of Mnemonic Anosognosia in the Aging Brain
Bueichekú E, Diez I, Gagliardi G, Kim C, Mimmack K, Sepulcre J, Vannini P. Multi‐modal Neuroimaging Phenotyping of Mnemonic Anosognosia in the Aging Brain. Alzheimer's & Dementia 2023, 19 DOI: 10.1002/alz.080294.Peer-Reviewed Original ResearchMnemonic anosognosiaOccipito-parietal regionsMemory declineBrain phenotypesSelf-referential brain networkObjective memory testsObjective memory declineResting-state fMRIPosterior cerebral cortexMulti-modal neuroimagingNetwork connectivity patternsAlzheimer's diseaseFunctional connectivity networksGraph theory metricsTau burdenNeurocognitive profileBiomarkers of AD pathologyMemory testMemory impairmentBetween-group comparisonsFunctional network connectivity disruptionBrain networksAging brainAnosognosiaBehavioral conditionsRelationship between loss of awareness of cognitive decline and tau pathology in the Alzheimer’s disease spectrum: modulatory role of resting‐state functional connectivity
Cacciamani F, Gagliardi G, Mimmack K, Qiao K, Bueichekú E, Marshall G, Sepulcre J, Diez I, Vannini P. Relationship between loss of awareness of cognitive decline and tau pathology in the Alzheimer’s disease spectrum: modulatory role of resting‐state functional connectivity. Alzheimer's & Dementia 2023, 19 DOI: 10.1002/alz.079806.Peer-Reviewed Original ResearchAwareness of cognitive declineResting-state functional connectivityLinear regression modelsSelf-referential networkHigher tau burdenFunctional connectivityCognitive declineRegression modelsTau accumulationAlzheimer's diseaseImpaired resting-state functional connectivityAlzheimer's disease spectrumResting-state fMRI dataAssociated with tau accumulationDorsal attention networkReduced awarenessWithin-network connectivityModulatory roleLow awarenessTau burdenEffects of tauCognitive function indicesTau interactionsSalience networkTau pathologyTau epicenter identification and connectivity in clinically heterogeneous Alzheimer’s disease variants
Trainer A, Xu W, Chase A, O'Dell R, Tun S, Li J, Ju S, van Dyck C, Mecca A, Fredricks C. Tau epicenter identification and connectivity in clinically heterogeneous Alzheimer’s disease variants. Alzheimer's & Dementia 2023, 19 DOI: 10.1002/alz.079435.Peer-Reviewed Original ResearchAmnestic Alzheimer's diseaseLogopenic variant primary progressive aphasiaPosterior cortical atrophyFunctional connectivity mapsHigher tau burdenFunctional connectivityTau burdenAlzheimer's diseaseConnectivity mapsLongitudinal tau-PETSpread of tauVariant primary progressive aphasiaFusiform gyrusFrontal eye fieldPrimary progressive aphasiaBrains of participantsTau PET scansSuperior parietal lobulePatient-specific biomarkersCortical atrophyCommon subtypeTau-PETHealthy controlsParietooccipital cortexPET scansCorrelations between APOE4 status and regional amyloid and tau burdens in cognitively normal older individuals
Hong Y, Kim C, Lee J, Sepulcre J. Correlations between APOE4 status and regional amyloid and tau burdens in cognitively normal older individuals. Alzheimer's & Dementia 2023, 19 DOI: 10.1002/alz.065023.Peer-Reviewed Original ResearchApolipoprotein epsilon 4Standardized uptake value ratioCarrier statusCortical thicknessPositron emission tomographyApolipoprotein epsilon 4 statusTau burdenCognitively normal older individualsAPOE4 carriersRegional amyloidNon-carriersCross-sectional studyNormal older individualsCognitively normal participantsFlorbetapir positron emission tomographyNormal cognitive functionAPOE4 non-carriersAssociated with amyloid depositionRegional tau burdenCognitive functionAD-related biomarkersAge differencesPhosphorylated tauNormal participantsClinical characteristics
2022
Correlations between APOE4 allele and regional amyloid and tau burdens in cognitively normal older individuals
Hong Y, Kim C, Lee J, Sepulcre J. Correlations between APOE4 allele and regional amyloid and tau burdens in cognitively normal older individuals. Scientific Reports 2022, 12: 14307. PMID: 35995824, PMCID: PMC9395408, DOI: 10.1038/s41598-022-18325-2.Peer-Reviewed Original ResearchConceptsApolipoprotein epsilon 4Apolipoprotein epsilon 4 alleleAlzheimer's Disease Neuroimaging InitiativeApolipoprotein epsilon 4 carriersTau burdenAmyloid depositsAPOE4 non-carriersAssociated with amyloid depositionPresence of ApoE4 alleleCross-sectional studyRegional tau burdenAssess correlationsCognitively normal participantsIncreased amyloid burdenNormal cognitive functionCognitively normal older individualsStandardized uptake value ratioEpsilon 4AD-related biomarkersAPOE4 alleleTau depositionCortical thicknessAmyloidCarrier statusAllelesAmyloid-β and tau pathologies relate to distinctive brain dysconnectomics in preclinical autosomal-dominant Alzheimer’s disease
Guzmán-Vélez E, Diez I, Schoemaker D, Pardilla-Delgado E, Vila-Castelar C, Fox-Fuller J, Baena A, Sperling R, Johnson K, Lopera F, Sepulcre J, Quiroz Y. Amyloid-β and tau pathologies relate to distinctive brain dysconnectomics in preclinical autosomal-dominant Alzheimer’s disease. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2113641119. PMID: 35380901, PMCID: PMC9169643, DOI: 10.1073/pnas.2113641119.Peer-Reviewed Original ResearchConceptsDefault-mode networkFunctional connectivitySalience networkRetrospenial cortexFunctional segregationPosterior default-mode networkAmyloid-bDefault-mode network regionsHigher-order cognitive functionsEarly-onset AD dementiaTau pathologyMedial prefrontal cortexAnterior cingulate cortexDisrupting neural communicationGraph-based network analysisBrain functional architectureMedial temporal regionsFunctional networksAlzheimer's diseaseBrain functional connectivityPreclinical Alzheimer's diseasePrefrontal cortexTau burdenCingulate cortexEpisodic memory
2021
Amyloid‐β and tau pathologies relate to distinctive brain dysconnectomics in autosomal‐dominant Alzheimer’s disease
Guzman‐Velez E, Diez I, Schoemaker D, Pardilla‐Delgado E, Fox‐Fuller J, Vila‐Castelar C, Baena A, Sperling R, Johnson K, Lopera F, Sepulcre J, Quiroz Y. Amyloid‐β and tau pathologies relate to distinctive brain dysconnectomics in autosomal‐dominant Alzheimer’s disease. Alzheimer's & Dementia 2021, 17 DOI: 10.1002/alz.056134.Peer-Reviewed Original ResearchAmyloid-bWeighted-degreesTau pathologyAutosomal-dominant Alzheimer's diseaseNon-carriersAutosomal-dominant ADTau burdenPredicting disease riskTau seedsPresenilin-1Tau propagationPSEN-1AD progressionSignificance thresholdAlzheimer's diseaseTauGraph-based network analysisMutation carriersTau-PETPosterior cingulate cortexMutationsConnectivity mapsGenetically-determinedResting-state fMRINetwork analysisTau‐Atrophy Variability Reveals Phenotypic Heterogeneity in Alzheimer's Disease
Das S, Lyu X, Duong M, Xie L, McCollum L, Flores R, DiCalogero M, Irwin D, Dickerson B, Nasrallah I, Yushkevich P, Wolk D, Weiner M, Aisen P, Petersen R, Jack C, Jagust W, Trojanowki J, Toga A, Beckett L, Green R, Saykin A, Morris J, Shaw L, Liu E, Montine T, Thomas R, Donohue M, Walter S, Gessert D, Sather T, Jiminez G, Harvey D, Donohue M, Bernstein M, Fox N, Thompson P, Schuff N, DeCArli C, Borowski B, Gunter J, Senjem M, Vemuri P, Jones D, Kantarci K, Ward C, Koeppe R, Foster N, Reiman E, Chen K, Mathis C, Landau S, Cairns N, Householder E, Reinwald L, Lee V, Korecka M, Figurski M, Crawford K, Neu S, Foroud T, Potkin S, Shen L, Kelley F, Kim S, Nho K, Kachaturian Z, Frank R, Snyder P, Molchan S, Kaye J, Quinn J, Lind B, Carter R, Dolen S, Schneider L, Pawluczyk S, Beccera M, Teodoro L, Spann B, Brewer J, Vanderswag H, Fleisher A, Heidebrink J, Lord J, Petersen R, Mason S, Albers C, Knopman D, Johnson K, Doody R, Meyer J, Chowdhury M, Rountree S, Dang M, Stern Y, Honig L, Bell K, Ances B, Morris J, Carroll M, Leon S, Householder E, Mintun M, Schneider S, Oliver A, Marson D, Griffith R, Clark D, Geld‐Macher D, Brockington J, Roberson E, Grossman H, Mitsis E, Toledo‐Morrell L, Shah R, Duara R, Varon D, Greig M, Roberts P, Albert M, Onyike C, D'Agostino D, Kielb S, Galvin J, Pogorelec D, Cerbone B, Michel C, Rusinek H, Leon M, Glodzik L, De Santi S, Doraiswamy P, Petrella J, Wong T, Arnold S, Karlawish J, Wolk D, Smith C, Jicha G, Hardy P, Sinha P, Oates E, Conrad G, Lopez O, Oakley M, Simpson D, Porsteinsson A, Goldstein B, Martin K, Makino K, Ismail M, Brand C, Mulnard R, Thai G, Ortiz C, Womack K, Mathers D, Quiceno M, Arrastia R, King R, Weiner M, Martin Cook K, DeVous M, Levey A, Lah J, Cellar J, Bums J, Anderson H, Swerdlow R, Apostolova L, Tingus K, Woo E, Silverman D, Lu P, Bartzokis G, Graff Radford N, Parfitt F, Kendall T, Johnson H, Farlow M, Hake A, Matthews B, Herring S, Hunt C, Dyck C, Carson R, MacAvoy M, Chertkow H, Bergman H, Hosein C, Black S, Stefanovic B, Caldwell C, Hsiung G, Feldman H, Mudge B, Assaly M, Kertesz A, Rogers J, Trost D, Bernick C, Munic D, Kerwin D, Mesulam M, Lipowski K, Wu C, Johnson N, Sadowsky C, Martinez W, Villena T, Turner R, Kathleen Johnson N, Brigid Reynolds N, Sperling R, Johnson K, Marshall G, Frey M, Yesavage J, Taylor J, Lane B, Rosen A, Tinklenberg J, Sabbagh M, Belden C, Jacobson S, Sirrel S, Kowall N, Killiany R, Budson A, Norbash A, Johnson P, Obisesan T, Wolday S, Allard J, Lerner A, Ogrocki P, Hudson L, Fletcher E, Carmichael O, Olichney J, DeCarli C, Kittur S, Borrie M, Lee T, Bartha R, Johnson S, Asthana S, Carlsson C, Potkin S, Preda A, Nguyen D, Tariot P, Fleisher A, Reeder S, Bates V, Capote H, Rainka M, Scharre D, Kataki M, Adeli A, Zimmerman E, Celmins D, Brown A, Pearlson G, Blank K, Anderson K, Santulli R, Kitzmiller T, Schwartz E, Sink K, Williamson J, Garg P, Watkins F, Ott B, Querfurth H, Tremont G, Salloway S, Malloy P, Correia S, Rosen H, Miller B, Mintzer J, Spicer K, Bachman D, Finger E, Pasternak S, Rachinsky I, Rogers J, Kertesz A, Drost D, Pomara N, Hernando R, Sarrael A, Schultz S, Boles Ponto L, Shim H, Smith K, Relkin N, Chaing G, Raudin L, Smith A, Fargher K, Raj B. Tau‐Atrophy Variability Reveals Phenotypic Heterogeneity in Alzheimer's Disease. Annals Of Neurology 2021, 90: 751-762. PMID: 34617306, PMCID: PMC8841129, DOI: 10.1002/ana.26233.Peer-Reviewed Original ResearchConceptsData-driven subgroupsAlzheimer's diseaseLow atrophyCortical thicknessBrain regionsWhite matter hyperintensity lesionsModulatory factorsAmyloid-positive individualsSubsequent cognitive impairmentLevels of tauGray matter regionsAnn NeurolDownstream neurodegenerationHyperintensity lesionsTau neurofibrillaryTau burdenClinical trialsCognitive impairmentMatter regionsDiseaseMultiple underlying factorsNeurodegenerationAtrophyCohortSUVRSpreading of Alzheimer tau seeds is enhanced by aging and template matching with limited impact of amyloid-β
Nies SH, Takahashi H, Herber CS, Huttner A, Chase A, Strittmatter SM. Spreading of Alzheimer tau seeds is enhanced by aging and template matching with limited impact of amyloid-β. Journal Of Biological Chemistry 2021, 297: 101159. PMID: 34480901, PMCID: PMC8477193, DOI: 10.1016/j.jbc.2021.101159.Peer-Reviewed Original ResearchConceptsTau seedsAlzheimer's diseaseAD model miceWT mouse brainPathological tauSynaptic lossTau accumulationWT miceMouse tauTau pathologyTau burdenModel miceTau inclusionsPharmacological interventionsAD riskCognitive declineMouse brainTau aggregatesPyk2 kinaseKnowledge of factorsKinase inhibitorsMiceFyn kinase inhibitorAβMouse aging
2017
[F-18]-AV-1451 binding correlates with postmortem neurofibrillary tangle Braak staging
Marquié M, Siao Tick Chong M, Antón-Fernández A, Verwer E, Sáez-Calveras N, Meltzer A, Ramanan P, Amaral A, Gonzalez J, Normandin M, Frosch M, Gómez-Isla T. [F-18]-AV-1451 binding correlates with postmortem neurofibrillary tangle Braak staging. Acta Neuropathologica 2017, 134: 619-628. PMID: 28612291, PMCID: PMC5772971, DOI: 10.1007/s00401-017-1740-8.Peer-Reviewed Original ResearchConceptsNeurofibrillary tanglesNeurofibrillary tau pathologyTau burdenBraak stageStaging of neurofibrillary tanglesBrain regionsAccurate diagnosis of Alzheimer's diseaseTau pathologyPhospho-tauStereotyped spatiotemporal patternBraak NFT stageNeurofibrillary tangle Braak stagePhosphor-screen autoradiographyAlzheimer's diseaseMild cognitive impairmentTau measuresNFT stageCognitively normal controlsObserved patternBraakCognitive impairmentWestern blottingBindingDiagnosis of Alzheimer's diseaseBraak staging of neurofibrillary tangles
2016
P4‐351: Evaluation of TAU Burden in a Cross‐Sectional Cohort of Alzheimer’S Disease Subjects Using [18F]GTP1 (GENENTECH TAU PROBE 1)
Bohorquez S, Barret O, Tamagnan G, Alagille D, Marik J, Ayalon G, Bengtsson T, de Crespigny A, Jennings D, Seibyl J, Marek K, Weimer R, Kerchner G. P4‐351: Evaluation of TAU Burden in a Cross‐Sectional Cohort of Alzheimer’S Disease Subjects Using [18F]GTP1 (GENENTECH TAU PROBE 1). Alzheimer's & Dementia 2016, 12: p1172-p1172. DOI: 10.1016/j.jalz.2016.07.096.Peer-Reviewed Original Research
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