2022
Neuroinflammation in neuronopathic Gaucher disease: Role of microglia and NK cells, biomarkers, and response to substrate reduction therapy
Boddupalli CS, Nair S, Belinsky G, Gans J, Teeple E, Nguyen TH, Mehta S, Guo L, Kramer ML, Ruan J, Wang H, Davison M, Kumar D, Vidyadhara D, Zhang B, Klinger K, Mistry PK. Neuroinflammation in neuronopathic Gaucher disease: Role of microglia and NK cells, biomarkers, and response to substrate reduction therapy. ELife 2022, 11: e79830. PMID: 35972072, PMCID: PMC9381039, DOI: 10.7554/elife.79830.Peer-Reviewed Original ResearchConceptsNeuronopathic Gaucher diseaseAmelioration of neuroinflammationNK cellsGaucher diseaseSerum neurofilament light chainInvolvement of microgliaActivation of microgliaRole of microgliaProminent pathological featureNeurofilament light chainBlood-derived macrophagesRare neurodegenerative disorderGlucosylceramide synthaseNeuroinflammation pathwaysSerum NFMicroglia activationNeuronal injuryImmune infiltratesImproved survivalBrain macrophagesPathological featuresGD patientsClinical trialsMacrophage compartmentPatient management
2020
IL-33-PU.1 Transcriptome Reprogramming Drives Functional State Transition and Clearance Activity of Microglia in Alzheimer’s Disease
Lau S, Chen C, Fu W, Qu J, Cheung T, Fu A, Ip N. IL-33-PU.1 Transcriptome Reprogramming Drives Functional State Transition and Clearance Activity of Microglia in Alzheimer’s Disease. Cell Reports 2020, 31: 107530. PMID: 32320664, DOI: 10.1016/j.celrep.2020.107530.Peer-Reviewed Original ResearchConceptsTranscriptome profilingAlzheimer's diseaseTranscription factor bindingSignature genesMicroglial state transitionChromatin accessibilityFactor bindingTranscriptome reprogrammingClearance activityBeta-amyloidTranscriptomeAD pathologyMicroglial transcriptomeTranscriptional pathwaysMajor histocompatibility complex classMicroglial subpopulationsTranscriptomic signaturesEnhanced phagocytic activityMicroglial functionHistocompatibility complex classPhagocytic activityAlzheimerInterleukin (IL)-33Activation of microgliaChromatin
2019
FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation
Yao S, Li L, Sun X, Hua J, Zhang K, Hao L, Liu L, Shi D, Zhou H. FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation. Journal Of Neuroimmune Pharmacology 2019, 14: 478-492. PMID: 31069623, DOI: 10.1007/s11481-019-09843-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntiparkinson AgentsApoptosisCell LineCorpus StriatumCytokinesDopaminergic NeuronsDrug Evaluation, PreclinicalExploratory BehaviorFingolimod HydrochlorideInflammasomesMaleMiceMice, Inbred C57BLMicrogliaMitochondriaMPTP PoisoningNeuroprotective AgentsNLR Family, Pyrin Domain-Containing 3 ProteinParkinsonian DisordersPars CompactaReactive Oxygen SpeciesRotarod Performance TestSignal TransductionConceptsTherapeutic effects of FTY720Effect of FTY720Therapeutic effectNLRP3 inflammasome activationDopaminergic neuronsMicroglial activationP65 activationInflammasome activationSubcutaneous injection of MPTPMPTP-induced microglial activationIncreased dopamine releaseMPTP-induced behavioral deficitsDamage to dopaminergic neuronsTumor necrosis factor-aAnimal models of PDInjection of MPTPROS generationSubstantia nigra pars compactaDecreased NLRP3 inflammasome activationParkinson's diseaseInterleukin (IL)-6Production of interleukin (IL)-6Degeneration of dopaminergic neuronsLoss of dopaminergic neuronsActivation of microglia
2018
Minocycline does not affect experimental pain or addiction-related outcomes in opioid maintained patients
Arout CA, Waters AJ, MacLean RR, Compton P, Sofuoglu M. Minocycline does not affect experimental pain or addiction-related outcomes in opioid maintained patients. Psychopharmacology 2018, 236: 2857-2866. PMID: 30564869, PMCID: PMC6581631, DOI: 10.1007/s00213-018-5146-7.Peer-Reviewed Original ResearchConceptsOpioid-induced hyperalgesiaCold pressor testOpioid use disorderSerum cytokinesPain thresholdUse disordersAddiction-related outcomesProinflammatory serum cytokinesActivation of microgliaSeverity of painEcological momentary assessmentEnd of treatmentHuman laboratory studiesTest sessionsOpioid cravingMinocycline treatmentOpioid toleranceAgonist treatmentPain sensitivityVisit 1Minocycline effectsPressor testExperimental painPreclinical studiesGo/No-Go task
2017
Abstract TP83: Stress Exacerbates Global Ischemia-induced Inflammatory Response: Intervention by Progesterone
Espinosa-Garcia C, Sayeed I, Yousuf S, Atif F, Sergeeva E, Neigh G, Stein D. Abstract TP83: Stress Exacerbates Global Ischemia-induced Inflammatory Response: Intervention by Progesterone. Stroke 2017, 48 DOI: 10.1161/str.48.suppl_1.tp83.Peer-Reviewed Original ResearchPro-inflammatory cytokinesNeuronal lossExposed to social defeat stressGlobal ischemiaIncreased brain-derived neurotrophic factor expressionInflammatory responsePost-ischemiaFactor expressionPost-ischemic inflammatory responseBrain-derived neurotrophic factor expressionAssociated with increased riskSocial defeat stressIschemia-induced inflammatory responseAdult male ratsAssociated with increased risk of strokeFour-vessel occlusion modelNeurotrophic factor expressionGrowth factor expressionHippocampal CA1 regionGlobal ischemic injuryActivation of microgliaExacerbated microglial activationRisk of strokeDays post-ischemiaDefeat stress
2016
Neurovascular unit remodelling in the subacute stage of stroke recovery
Lake EMR, Bazzigaluppi P, Mester J, Thomason LAM, Janik R, Brown M, McLaurin J, Carlen PL, Corbett D, Stanisz GJ, Stefanovic B. Neurovascular unit remodelling in the subacute stage of stroke recovery. NeuroImage 2016, 146: 869-882. PMID: 27664828, DOI: 10.1016/j.neuroimage.2016.09.016.Peer-Reviewed Original ResearchConceptsPeri-lesional cortexVascular reactivityNeuronal lossSubacute stageEndothelin-1LFP activityLong-term functional outcomeLocal field potential responsesPeripheral somatosensory stimulationActivation of microgliaET-1 injectionFocal ischemic strokeFocal cerebral ischaemiaPeri-infarct zoneSensori-motor cortexSpontaneous neuronal activityAdult Sprague-DawleyField potential responsesExtended temporal windowDynamic functional changesIschemic strokeAstrocytic activationCerebral ischaemiaNeurovascular unitIschemic insult
2015
Imaging robust microglial activation after lipopolysaccharide administration in humans with PET
Sandiego CM, Gallezot JD, Pittman B, Nabulsi N, Lim K, Lin SF, Matuskey D, Lee JY, O’Connor K, Huang Y, Carson RE, Hannestad J, Cosgrove KP. Imaging robust microglial activation after lipopolysaccharide administration in humans with PET. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 12468-12473. PMID: 26385967, PMCID: PMC4603509, DOI: 10.1073/pnas.1511003112.Peer-Reviewed Original ResearchConceptsMicroglial activationBrain microglial activationLPS administrationInflammatory cytokinesLPS challengeRobust microglial activationSystemic LPS challengeActivation of microgliaInnate immune cellsVital sign changesHealthy male subjectsEscherichia coli lipopolysaccharidePositron emission tomography (PET) radiotracerNeuroinflammatory responseSystemic inflammationLipopolysaccharide administrationAntiinflammatory effectsBlood levelsImmune cellsNew medicationsSystemic administrationColi lipopolysaccharidePET scansPsychiatric diseasesMale subjects
2014
Microglial CX3CR1 required for M2 polarization and recovery after intracerebral hemorrhage (INC5P.322)
Taylor R, Hammond M, Ai Y, Sansing L. Microglial CX3CR1 required for M2 polarization and recovery after intracerebral hemorrhage (INC5P.322). The Journal Of Immunology 2014, 192: 120.2-120.2. DOI: 10.4049/jimmunol.192.supp.120.2.Peer-Reviewed Original ResearchIntracerebral hemorrhageBeam walkingWT microgliaIntracellular stainingCX3CR1GFP/GFP miceHigher CD36 expressionActivation of microgliaBone marrow chimerasBrain rupturesMicroglial CX3CR1IL-10WT micePerihematomal regionMonocyte subsetsIL-4Right striatumChemokine receptorsM1 phenotypeM2 polarizationM2 phenotypeMicrogliaCD36 expressionBone marrowNull miceGFP mice
2013
The neuroinflammation marker translocator protein is not elevated in individuals with mild-to-moderate depression: A [11C]PBR28 PET study
Hannestad J, DellaGioia N, Gallezot JD, Lim K, Nabulsi N, Esterlis I, Pittman B, Lee JY, O’Connor K, Pelletier D, Carson RE. The neuroinflammation marker translocator protein is not elevated in individuals with mild-to-moderate depression: A [11C]PBR28 PET study. Brain Behavior And Immunity 2013, 33: 131-138. PMID: 23850810, PMCID: PMC3899398, DOI: 10.1016/j.bbi.2013.06.010.Peer-Reviewed Original ResearchConceptsLevels of TSPOControl subjectsSystemic inflammationPositron emission tomographyModerate depressionTSPO levelsActivation of microgliaTranslocator protein 18Total ligand bindingAcute episodePrimary outcomePostmortem studiesSevere depressionMajor depressionPET scansTSPO genotypeBrain regionsEmission tomographySubject factorsPET studiesArterial input functionInflammationElevated levelsProtein 18Depression
2012
Endotoxin-induced systemic inflammation activates microglia: [11C]PBR28 positron emission tomography in nonhuman primates
Hannestad J, Gallezot JD, Schafbauer T, Lim K, Kloczynski T, Morris ED, Carson RE, Ding YS, Cosgrove KP. Endotoxin-induced systemic inflammation activates microglia: [11C]PBR28 positron emission tomography in nonhuman primates. NeuroImage 2012, 63: 232-239. PMID: 22776451, PMCID: PMC3699786, DOI: 10.1016/j.neuroimage.2012.06.055.Peer-Reviewed Original ResearchConceptsPositron emission tomographySystemic inflammationMultiple sclerosisInterleukin-6Interleukin-8Translocator proteinEndotoxin-induced systemic inflammationLevels of TSPOEmission tomographyTumor necrosis factor alphaSystemic inflammatory processActivation of microgliaSerum IL-1βIL-6 levelsCourse of diseaseEffects of LPSImportant clinical questionsNecrosis factor alphaInterleukin-1 betaNonhuman primate brainE. coli lipopolysaccharideRegional time-activity dataLocal tissue damageTwo-tissue compartmental modelTotal ligand binding
2009
Unilateral Focal Burn Injury Is Followed by Long-Lasting Bilateral Allodynia and Neuronal Hyperexcitability in Spinal Cord Dorsal Horn
Chang YW, Tan A, Saab C, Waxman S. Unilateral Focal Burn Injury Is Followed by Long-Lasting Bilateral Allodynia and Neuronal Hyperexcitability in Spinal Cord Dorsal Horn. Journal Of Pain 2009, 11: 119-130. PMID: 19744891, DOI: 10.1016/j.jpain.2009.06.009.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnalysis of VarianceAnimalsBrain InjuriesCalcitonin Gene-Related PeptideCD11b AntigenDisease Models, AnimalFunctional LateralityHyperesthesiaMaleMicrogliap38 Mitogen-Activated Protein KinasesPainPain MeasurementPain ThresholdPhysical StimulationPosterior Horn CellsRatsSpinal CordSubstance PConceptsSpinal cord dorsal hornBurn injuryBurn injury modelBilateral allodyniaDorsal hornNeuronal hyperexcitabilityInjury modelSpinal cordDorsal horn neuronal hyperexcitabilitySecond-order sensory neuronsCentral neuropathic mechanismsIpsilateral mechanical allodyniaDorsal horn neuronsActivation of microgliaPathogenesis of painPotential therapeutic targetNovel animal modelContralateral allodyniaMechanical allodyniaNeuropathic mechanismsSpinal microgliaBilateral painMicroglial activationNerve injuryWeeks postinjury
2004
Sodium channels contribute to microglia/macrophage activation and function in EAE and MS
Craner MJ, Damarjian TG, Liu S, Hains BC, Lo AC, Black JA, Newcombe J, Cuzner ML, Waxman SG. Sodium channels contribute to microglia/macrophage activation and function in EAE and MS. Glia 2004, 49: 220-229. PMID: 15390090, DOI: 10.1002/glia.20112.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGliosisMacrophagesMaleMiceMice, Inbred C57BLMicrogliaMultiple SclerosisNAV1.6 Voltage-Gated Sodium ChannelNerve DegenerationNerve Tissue ProteinsNeuroprotective AgentsPhagocytosisPhenytoinRNA, MessengerSodium Channel BlockersSodium ChannelsTetrodotoxinUp-RegulationConceptsExperimental autoimmune encephalomyelitisMultiple sclerosisSodium channel blockersSodium channelsMicroglial activationChannel blockersPhagocytic capacityMicroglia/macrophage activationSpecific sodium channel blockerAcute MS lesionsDirect neuroprotective effectsPhagocytosis of microgliaActivation of microgliaAnti-inflammatory mechanismsSodium channel-blocking drugsInflammatory cell infiltrateLoss of axonsDisease multiple sclerosisSodium channel blockadeChannel-blocking drugsAxonal sodium channelsAutoimmune encephalomyelitisInflammatory mechanismsNeuroinflammatory disordersCell infiltrate
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
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