2021
Chapter 15 Positron emission tomography imaging agents for evaluating the pathologic features of Alzheimer's disease and drug development
Huang Y, Jia H, Bao W. Chapter 15 Positron emission tomography imaging agents for evaluating the pathologic features of Alzheimer's disease and drug development. 2021, 367-412. DOI: 10.1016/b978-0-12-816475-4.00013-6.Peer-Reviewed Original ResearchAlzheimer's diseasePathologic featuresApplication of PETDrug developmentSynaptic vesicle protein 2ADifferent pathologic featuresFeatures of neurodegenerationCentral nervous systemAD drug developmentPositron emission tomographyNeuroinflammation biomarkersCholinergic systemΒ-amyloidNervous systemTau proteinEmission tomographyAD researchDiseaseProtein 2AInvestigation of diseasesQuantitative imaging techniquesTomographyImaging techniquesAgentsPET
2019
Short-term high-fat diet modulates several inflammatory, ER stress, and apoptosis markers in the hippocampus of young mice
Nakandakari S, Muñoz V, Kuga G, Gaspar R, Sant'Ana M, Pavan I, da Silva L, Morelli A, Simabuco F, da Silva A, de Moura L, Ropelle E, Cintra D, Pauli J. Short-term high-fat diet modulates several inflammatory, ER stress, and apoptosis markers in the hippocampus of young mice. Brain Behavior And Immunity 2019, 79: 284-293. PMID: 30797044, DOI: 10.1016/j.bbi.2019.02.016.Peer-Reviewed Original ResearchConceptsHigh-fat dietYoung miceShort-term HFD feedingMice fed high-fat dietFed high-fat dietHippocampus of miceER stressDisease developmentShort-term consumptionAlzheimer's disease developmentPotential molecular mechanismsHOMA-IRHFD feedingAD markersMicroglial cellsAD pathogenesisRisk factorsInflammatory signalsDiet modulatesΒ-amyloidCleaved caspase3HippocampusApoptosis markersHigh expressionMice
2017
Phosphorylated Presenilin 1 decreases β-amyloid by facilitating autophagosome–lysosome fusion
Bustos V, Pulina MV, Bispo A, Lam A, Flajolet M, Gorelick FS, Greengard P. Phosphorylated Presenilin 1 decreases β-amyloid by facilitating autophagosome–lysosome fusion. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: 7148-7153. PMID: 28533369, PMCID: PMC5502640, DOI: 10.1073/pnas.1705240114.Peer-Reviewed Original ResearchAbsence of Alzheimer Disease Neuropathologic Changes in Eyes of Subjects With Alzheimer Disease
Williams EA, McGuone D, Frosch MP, Hyman BT, Laver N, Stemmer-Rachamimov A. Absence of Alzheimer Disease Neuropathologic Changes in Eyes of Subjects With Alzheimer Disease. Journal Of Neuropathology & Experimental Neurology 2017, 76: 376-383. PMID: 28379416, PMCID: PMC7191616, DOI: 10.1093/jnen/nlx020.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseMacular degenerationΒ-amyloidAlzheimer's disease neuropathologic changeAD-related changesAge-matched controlsEyes of subjectsAD-related featuresSeverity of changesAlzheimer changesNeuropathologic changesPathologic findingsAutopsy casesVisual deficitsCommon causeTDP-43Pathology studiesTau proteinExtracellular depositionΑ-synucleinIntracellular accumulationBrainSimilar changesDegenerationDisease
2016
β-Amyloid, APOE and BDNF Genotype, and Depressive and Anxiety Symptoms in Cognitively Normal Older Women and Men
Holmes SE, Esterlis I, Mazure CM, Lim YY, Ames D, Rainey-Smith S, Martins RN, Salvado O, Dore V, Villemagne VL, Rowe CC, Laws SM, Masters CL, Maruff P, Pietrzak RH, Australian Imaging B. β-Amyloid, APOE and BDNF Genotype, and Depressive and Anxiety Symptoms in Cognitively Normal Older Women and Men. American Journal Of Geriatric Psychiatry 2016, 24: 1191-1195. PMID: 27742526, DOI: 10.1016/j.jagp.2016.08.007.Peer-Reviewed Original ResearchConceptsBDNF genotypeNormal older womenAnxiety symptomsOlder adultsΕ4 carriageOlder womenDepressive symptomsΒ-amyloidGreater severityAustralian Imaging BiomarkersNon-ε4 carriersSeverity of depressiveMet allele carriersSeverity of anxietyGreater depressive symptomsNormal older adultsGreater anxiety symptomsLifestyle StudyΕ4 carriersAPOE genotypeAllele carriersAnalysis of covarianceImaging biomarkersSymptomsDepressivePolygenic risk of Alzheimer disease is associated with early- and late-life processes
Mormino EC, Sperling RA, Holmes AJ, Buckner RL, De Jager PL, Smoller JW, Sabuncu MR, Weiner M, Aisen P, Weiner M, Aisen P, Petersen R, Jack C, Jagust W, Trojanowki J, Toga A, Beckett L, Green R, Saykin A, Morris J, Liu E, Green R, Montine T, Petersen R, Aisen P, Gamst A, Thomas R, Donohue M, Walter S, Gessert D, Sather T, Beckett L, Harvey D, Gamst A, Donohue M, Kornak J, Jack C, Dale A, Bernstein M, Felmlee J, Fox N, Thompson P, Schuff N, Alexander G, DeCarli C, Jagust W, Bandy D, Koeppe R, Foster N, Reiman E, Chen K, Mathis C, Morris J, Cairns N, Taylor-Reinwald L, Trojanowki J, Shaw L, Lee V, Korecka M, Toga A, Crawford K, Neu S, Saykin A, Foroud T, Potkin S, Shen L, Kachaturian Z, Frank R, Snyder P, Molchan S, Kaye J, Quinn J, Lind B, Dolen S, Schneider L, Pawluczyk S, Spann B, Brewer J, Vanderswag H, Heidebrink J, Lord J, Petersen R, Johnson K, Doody R, Villanueva-Meyer J, Chowdhury M, Stern Y, Honig L, Bell K, Morris J, Ances B, Carroll M, Leon S, Mintun M, Schneider S, Marson D, Griffith R, Clark D, Grossman H, Mitsis E, Romirowsky A, deToledo-Morrell L, Shah R, Duara R, Varon D, Roberts P, Albert M, Onyike C, Kielb S, Rusinek H, de Leon M, Glodzik L, De Santi S, Doraiswamy P, Petrella J, Coleman R, Arnold S, Karlawish J, Wolk D, Smith C, Jicha G, Hardy P, Lopez O, Oakley M, Simpson D, Porsteinsson A, Goldstein B, Martin K, Makino K, Ismail M, Brand C, Mulnard R, Thai G, Mc-Adams-Ortiz C, Womack K, Mathews D, Quiceno M, Diaz-Arrastia R, King R, Weiner M, Martin-Cook K, DeVous M, Levey A, Lah J, Cellar J, Burns J, Anderson H, Swerdlow R, Apostolova L, Lu P, Bartzokis G, Silverman D, Graff-Radford N, Parfitt F, Johnson H, Farlow M, Hake A, Matthews B, Herring S, van Dyck C, Carson R, MacAvoy M, Chertkow H, Bergman H, Hosein C, Black S, Stefanovic B, Caldwell C, Robin 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, Johnson K, Reynolds B, Sperling R, Johnson K, Marshall G, Frey M, Yesavage J, Taylor J, Lane B, Rosen A, Tinklenberg J, Sabbagh M, Belden C, Jacobson S, Kowall N, Killiany R, Budson A, Norbash A, Johnson P, Obisesan T, Wolday S, Bwayo S, Lerner A, Hudson L, Ogrocki P, Fletcher E, Carmichael O, Olichney J, DeCarli C, Kittur S, Borrie M, Lee T, Bartha D, 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, Zimmerman E, Celmins D, Brown A, Pearlson G, Blank K, Anderson K, Saykin A, Santulli R, 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, Longmire C, Spicer K, Finger E, 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. Polygenic risk of Alzheimer disease is associated with early- and late-life processes. Neurology 2016, 87: 481-488. PMID: 27385740, PMCID: PMC4970660, DOI: 10.1212/wnl.0000000000002922.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAlzheimer DiseaseAmyloid beta-PeptidesAniline CompoundsAtrophyBiomarkersCognition DisordersCohort StudiesEarly DiagnosisEthylene GlycolsFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHippocampusHumansMaleMemory DisordersMultifactorial InheritancePolymorphism, Single NucleotidePositron-Emission TomographyYoung AdultConceptsHigher polygenic risk scorePolygenic risk scoresHippocampus volumeRisk scoreLarge observational cohort studyCommon genetic risk lociSmaller hippocampus volumesΒ-amyloid burdenObservational cohort studyGenetic riskElevated polygenic risk scoresAlzheimer's disease markersCSF β-amyloidLongitudinal cognitive declineHealthy young participantsCohort studyClinical progressionClinical symptomsAD dementiaAD markersSmaller hippocampiFlorbetapir PETAggregate genetic riskΒ-amyloidGenome-wide association studiesAccelerating rates of cognitive decline and imaging markers associated with &bgr;-amyloid pathology
Insel P, Mattsson N, Mackin R, Schöll M, Nosheny R, Tosun D, Donohue M, Aisen P, Jagust W, Weiner M, Weiner M, Aisen P, Weiner M, Aisen P, Petersen R, Jack C, Jagust W, Trojanowki J, Toga A, Beckett L, Green R, Saykin A, Morris J, Liu E, Green R, Montine T, Petersen R, Aisen P, Gamst A, Thomas R, Donohue M, Walter S, Gessert D, Sather T, Beckett L, Harvey D, Gamst A, Donohue M, Kornak J, Jack C, Dale A, Bernstein M, Felmlee J, Fox N, Thompson P, Schuff N, Alexander G, DeCarli C, Jagust W, Bandy D, Koeppe R, Foster N, Reiman E, Chen K, Mathis C, Morris J, Cairns N, Taylor-Reinwald L, Trojanowki J, Shaw L, Lee V, Korecka M, Toga A, Crawford K, Neu S, Saykin A, Foroud T, Potkin S, Shen L, Kachaturian Z, Frank R, Snyder P, Molchan S, Kaye J, Quinn J, Lind B, Dolen S, Schneider L, Pawluczyk S, Spann B, Brewer J, Vanderswag H, Heidebrink J, Lord J, Petersen R, Johnson K, Doody R, Villanueva-Meyer J, Chowdhury M, Stern Y, Honig L, Bell K, Morris J, Ances B, Carroll M, Leon S, Mintun M, Schneider S, Marson D, Griffith R, Clark D, Grossman H, Mitsis E, Romirowsky A, deToledo-Morrell L, Shah R, Duara R, Varon D, Roberts, CNA P, Albert M, Onyike C, Kielb S, Rusinek H, de Leon M, Glodzik L, De Santi S, Doraiswamy P, Petrella J, Coleman R, Arnold S, Karlawish J, Wolk D, Smith C, Jicha G, Hardy P, Lopez O, Oakley M, Simpson D, Porsteinsson A, Goldstein B, Martin K, Makino K, Ismail M, Brand C, Mulnard R, Thai G, Mc-Adams-Ortiz C, Womack K, Mathews D, Quiceno M, Diaz-Arrastia R, King R, Weiner M, Martin-Cook K, DeVous M, Levey A, Lah J, Cellar J, Burns J, Anderson H, Swerdlow R, Apostolova L, Lu P, Bartzokis G, Silverman D, Graff-Radford, MBBCH N, Parfitt F, Johnson H, Farlow M, Hake A, Matthews B, Herring S, van Dyck C, Carson R, MacAvoy M, Chertkow H, Bergman H, Hosein C, Black S, Stefanovic B, Caldwell C, Robin 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, Johnson K, Reynolds B, Sperling R, Johnson K, Marshall G, Frey M, Yesavage J, Taylor J, Lane B, Rosen A, Tinklenberg J, Sabbagh M, Belden C, Jacobson S, Kowall N, Killiany R, Budson A, Norbash A, Johnson P, Obisesan T, Wolday S, Bwayo S, Lerner A, Hudson L, Ogrocki P, 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, Zimmerman E, Celmins D, Brown A, Pearlson G, Blank K, Anderson K, Saykin A, Santulli R, 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, Longmire C, Spicer K, Finger E, Rachinsky I, Rogers J, Kertesz A, Drost D, Pomara N, Hernando R, Sarrael A, Schultz S, Boles Ponto L, Shim H, Elizabeth Smith K, Relkin N, Chaing G, Raudin L, Smith A, Fargher K, Ashok Raj B. Accelerating rates of cognitive decline and imaging markers associated with &bgr;-amyloid pathology. Neurology 2016, 86: 1887-1896. PMID: 27164667, PMCID: PMC4873684, DOI: 10.1212/wnl.0000000000002683.Peer-Reviewed Original ResearchMeSH KeywordsAgedAmyloid beta-PeptidesAniline CompoundsAtrophyBiomarkersBrainCognitionCognitive DysfunctionDisease ProgressionEthylene GlycolsFemaleFluorodeoxyglucose F18HumansLongitudinal StudiesMagnetic Resonance ImagingMaleMental Status ScheduleNeuropsychological TestsPeptide FragmentsPositron-Emission TomographyRadiopharmaceuticalsRegression AnalysisConceptsMild cognitive impairmentFunctional declineNeuronal injuryCSF Aβ42Florbetapir PETAmyloid positivityRate of declineCognitive declineTemporal lobe atrophy ratesΒ-amyloid pathologyEarly Alzheimer's diseaseFluorodeoxyglucose PETAmyloid pathologyFDG-PETFuture trialsAtrophy ratesInclusion criteriaMixed-effects regressionΒ-amyloidCognitive impairmentAlzheimer's diseaseFirst signPatientsInjuryConsiderable proportion
2006
Role of p21-activated kinase pathway defects in the cognitive deficits of Alzheimer disease
Zhao L, Ma QL, Calon F, Harris-White ME, Yang F, Lim GP, Morihara T, Ubeda OJ, Ambegaokar S, Hansen JE, Weisbart RH, Teter B, Frautschy SA, Cole GM. Role of p21-activated kinase pathway defects in the cognitive deficits of Alzheimer disease. Nature Neuroscience 2006, 9: 234-242. PMID: 16415866, DOI: 10.1038/nn1630.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseCognitive deficitsDrebrin lossMental retardationP21-activated kinase pathwaysTransgenic mouse modelDendritic spine morphogenesisPotential causal roleP21-activated kinaseHippocampal neuronsDendritic spinesMouse modelΒ-amyloidAdult miceMemory impairmentDiseaseProtein drebrinSpine morphogenesisCausal roleCofilin pathologyDeficitsPAK pathwayPathologyPAK inhibitionKinase pathway
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