2025
CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models
Leser F, Júnyor F, Pagnoncelli I, Delgado A, Medeiros I, Nóbrega A, Andrade B, de Lima M, da Silva N, Jacob L, Boyé K, Geraldo L, de Souza A, Maron-Gutierrez T, Castro-Faria-Neto H, Follmer C, Braga C, Neves G, Eichmann A, Romão L, Lima F. CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models. Journal Of Neuroinflammation 2025, 22: 31. PMID: 39894839, PMCID: PMC11789347, DOI: 10.1186/s12974-024-03318-x.Peer-Reviewed Original ResearchConceptsMouse model of PDModel of PDMouse modelDopaminergic neuronsNeuron-microglia communicationNeuron-glia communicationParkinson's diseaseCCR7-dependent mannerMicroglial cell activationCCR7 expressionCCL21-CCR7Progressive degenerative diseaseCCR7 receptorMicroglial cell migrationInflammatory profileChemokine CCL21Cell activationCCL21Therapeutic strategiesChemokine inhibitorsTherapeutic implicationsMicroglial activationReceptor pathwayCCR7Behavioral deficits
2024
Parkinsonism Sac domain mutation in Synaptojanin-1 affects ciliary properties in iPSC-derived dopaminergic neurons
Rafiq N, Fujise K, Rosenfeld M, Xu P, De Camilli P. Parkinsonism Sac domain mutation in Synaptojanin-1 affects ciliary properties in iPSC-derived dopaminergic neurons. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2318943121. PMID: 38635628, PMCID: PMC11047088, DOI: 10.1073/pnas.2318943121.Peer-Reviewed Original ResearchConceptsSynaptojanin 1Endocytic factorsDA neuronsCilia-mediated signalingNerve terminalsIPSC-derived dopaminergic neuronsUbiquitin chainsUbiquitinated proteinsCiliary baseCilia lengthNeurological defectsDopaminergic neuronsProtein dynamicsDomain mutationsAssembly stateIsogenic controlsNeuronsAbnormal accumulationMutationsMiceFocal concentrationParkinsonPI(4UbiquitinEndocytosis
2023
Exploring therapeutic strategies for infantile neuronal axonal dystrophy (INAD/PARK14)
Lin G, Tepe B, McGrane G, Tipon R, Croft G, Panwala L, Hope A, Liang A, Zuo Z, Byeon S, Wang L, Pandey A, Bellen H. Exploring therapeutic strategies for infantile neuronal axonal dystrophy (INAD/PARK14). ELife 2023, 12: e82555. PMID: 36645408, PMCID: PMC9889087, DOI: 10.7554/elife.82555.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCeramidesDrosophilaDrosophila ProteinsEye ProteinsGroup VI Phospholipases A2MiceNeuroaxonal DystrophiesNeuronsParkinsonian DisordersConceptsPatient-derived neural progenitor cellsNeural progenitor cellsPatient-derived neuronsPediatric neurodegenerative disorderRetromer functionMitochondrial morphologyEndolysosomal pathwayMitochondrial defectsProlong lifespanNeurodegenerative phenotypeProgenitor cellsMouse modelRecessive variantsNeurodegenerative disordersGene therapy approachesPathwayInfantile neuroaxonal dystrophyHomologCellsTherapeutic strategiesAzoramidePurkinje cellsFliesPhenotypeMetabolism
2021
Immunomodifying and neuroprotective effects of noscapine: Implications for multiple sclerosis, neurodegenerative, and psychiatric disorders
Altinoz M, Guloksuz S, Ozpinar A. Immunomodifying and neuroprotective effects of noscapine: Implications for multiple sclerosis, neurodegenerative, and psychiatric disorders. Chemico-Biological Interactions 2021, 352: 109794. PMID: 34963564, DOI: 10.1016/j.cbi.2021.109794.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyotrophic Lateral SclerosisAnimalsBradykininHistamine AntagonistsHumansImmunomodulating AgentsIon ChannelsMental DisordersMultiple SclerosisNeurodegenerative DiseasesNeuroprotective AgentsNoscapineOligodendrogliaParkinsonian DisordersReceptors, G-Protein-CoupledSignal TransductionStrokeConceptsNeuroprotective effectsMultiple sclerosisInflammatory transcription factor NF-κBIschemic brain damageNeonatal rat pupsPilot clinical studyAmyotrophic lateral sclerosisTranscription factor NF-κBCortical neuronal cellsSignificant therapeutic efficacyFactor NF-κBBitter taste receptorsHistaminergic systemBrain damageRat pupsClinical studiesSK channelsLateral sclerosisParkinson's diseaseAnxiolytic activityPsychiatric disordersChemical injuryNF-κBAnimal modelsPsychiatric diseases
2020
A Splice Intervention Therapy for Autosomal Recessive Juvenile Parkinson’s Disease Arising from Parkin Mutations
Li D, Aung-Htut M, Ham K, Fletcher S, Wilton S. A Splice Intervention Therapy for Autosomal Recessive Juvenile Parkinson’s Disease Arising from Parkin Mutations. International Journal Of Molecular Sciences 2020, 21: 7282. PMID: 33019779, PMCID: PMC7582384, DOI: 10.3390/ijms21197282.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingBase SequenceExonsFibroblastsGene ExpressionGenetic TherapyHeterozygoteHumansMitochondriaMorpholinosOligonucleotides, AntisenseOpen Reading FramesParkinsonian DisordersPrecision MedicinePrimary Cell CultureRNA, MessengerSequence DeletionTumor Suppressor Protein p53Ubiquitin-Protein LigasesConceptsReading frameAutosomal recessive juvenile Parkinson diseaseInducing exon 4 skippingAntisense oligomersJuvenile-onset Parkinson's diseaseExon 4 skippingUbiquitin-proteasome systemMRNA reading frameGenomic deletionsE3 ligaseTranscriptional repressorJuvenile Parkinson's diseaseDepolarised mitochondriaExon 3 deletionParkin proteinExon 3Parkin isoformsParkin expressionParkin mutationsNeuroprotective proteinMutationsTranscriptionDeletionParkinIsoforms
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
Development of an aggregate-selective, human-derived α-synuclein antibody BIIB054 that ameliorates disease phenotypes in Parkinson's disease models
Weihofen A, Liu Y, Arndt JW, Huy C, Quan C, Smith BA, Baeriswyl JL, Cavegn N, Senn L, Su L, Marsh G, Auluck P, Montrasio F, Nitsch RM, Hirst WD, Cedarbaum JM, Pepinsky R, Grimm J, Weinreb PH. Development of an aggregate-selective, human-derived α-synuclein antibody BIIB054 that ameliorates disease phenotypes in Parkinson's disease models. Neurobiology Of Disease 2018, 124: 276-288. PMID: 30381260, DOI: 10.1016/j.nbd.2018.10.016.Peer-Reviewed Original ResearchMeSH Keywordsalpha-SynucleinAnimalsAntibodies, MonoclonalHumansMiceParkinsonian DisordersPhenotypeProtein AggregatesConceptsΑ-Syn pathologyParkinson's diseaseΑ-synDisease progressionMouse modelPrevention of PDPhase 2 clinical trialPD mouse modelPD brain tissueDisease modelsDopamine transporter densityParkinson's disease modelΑ-synuclein antibodyPromising therapeutic approachDifferent mouse modelsHealthy elderly individualsΑ-syn fibrilsEpitope mapping studiesDopaminergic terminalsRecombinant α-synPreclinical dataClinical trialsTherapeutic approachesMotor impairmentElderly individuals
2017
Parkinson Sac Domain Mutation in Synaptojanin 1 Impairs Clathrin Uncoating at Synapses and Triggers Dystrophic Changes in Dopaminergic Axons
Cao M, Wu Y, Ashrafi G, McCartney AJ, Wheeler H, Bushong EA, Boassa D, Ellisman MH, Ryan TA, De Camilli P. Parkinson Sac Domain Mutation in Synaptojanin 1 Impairs Clathrin Uncoating at Synapses and Triggers Dystrophic Changes in Dopaminergic Axons. Neuron 2017, 93: 882-896.e5. PMID: 28231468, PMCID: PMC5340420, DOI: 10.1016/j.neuron.2017.01.019.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsClathrinDopamineEndocytosisHumansMice, TransgenicMutationParkinson DiseaseParkinsonian DisordersPhosphoric Monoester HydrolasesSynapsesConceptsDopaminergic axonsEarly-onset parkinsonism patientsEndocytic dysfunctionNeurological manifestationsParkinsonism patientsDystrophic changesParkinson's diseaseDorsal striatumHuman patientsClathrin-coated intermediatesParkin levelsHomozygous mutationMutant brainsSynaptojanin 1Domain mutationsTerminal changesPatientsStriking accumulationAxonsDiseaseMiceSynapsesSynaptic vesicle endocytosisMutationsDysfunction
2016
Varied autopsy findings in five treated patients with Gaucher disease and parkinsonism include the absence of Gaucher cells
Monestime G, Borger DK, Kim J, Lopez G, Allgaeuer M, Jain D, Vortmeyer A, Wang HW, Sidransky E. Varied autopsy findings in five treated patients with Gaucher disease and parkinsonism include the absence of Gaucher cells. Molecular Genetics And Metabolism 2016, 118: 55-59. PMID: 26992326, DOI: 10.1016/j.ymgme.2016.02.008.Peer-Reviewed Original ResearchMeSH KeywordsAgedAutopsyDrug Administration ScheduleEnzyme Replacement TherapyFemaleGaucher DiseaseHumansMaleMiddle AgedParkinsonian DisordersTreatment OutcomeConceptsAutopsy findingsGaucher diseaseDose/durationEnzyme replacement therapySpleen statusPathological findingsReplacement therapyDisease burdenPathological studiesGaucher cellsPatientsHematological symptomsExtensive involvementTherapyParkinsonismDiseaseMultiple tissuesComplete absenceFindingsAutopsiesSymptomsPathologyBiomarkersCare
2015
Dopamine-dependent corticostriatal synaptic filtering regulates sensorimotor behavior
Wong MY, Borgkvist A, Choi SJ, Mosharov EV, Bamford NS, Sulzer D. Dopamine-dependent corticostriatal synaptic filtering regulates sensorimotor behavior. Neuroscience 2015, 290: 594-607. PMID: 25637802, PMCID: PMC4494866, DOI: 10.1016/j.neuroscience.2015.01.022.Peer-Reviewed Original ResearchConceptsReceptor agonistD2-like receptor agonistDopamine D2-like receptor agonistsSensorimotor responsesNigrostriatal dopamine axonsD2 receptor activationD2 receptor agonistCB1 receptor antagonistLeft dorsal striatumSensorimotor behaviorSynaptic filteringCB1 endocannabinoid receptorLesioned miceCorticostriatal terminalsCorticostriatal synapsesSensorimotor deficitsReplacement therapyD2 agonistMetabotropic glutamateReceptor antagonistCB1 receptorsEndocannabinoid receptorsSynaptic activityControl disordersCorticostriatal activity
2014
Intravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats
Suzuki S, Kawamata J, Iwahara N, Matsumura A, Hisahara S, Matsushita T, Sasaki M, Honmou O, Shimohama S. Intravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats. Neuroscience Letters 2014, 584: 276-281. PMID: 25449872, DOI: 10.1016/j.neulet.2014.10.039.Peer-Reviewed Original ResearchConceptsHuman bone marrow-derived mesenchymal stem cellsTherapeutic effectParkinson's diseaseCalcium binding adaptor molecule 1Mesenchymal stem cell administrationSubstantia nigra pars compactaHemi-parkinsonian rat modelParkinsonian model ratsTH-positive neuronsAdaptor molecule 1Anti-inflammatory factorsStem cell administrationNovel therapeutic optionsSham-operated ratsBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsGlial activationPars compactaCell administrationTherapeutic optionsDopaminergic neuronsModel ratsDopaminergic neurodegenerationNovel therapiesRat modelFBXO7–R498X mutation: Phenotypic variability from chorea to early onset parkinsonism within a family
Gündüz A, Eken A, Bilgiç B, Hanagasi HA, Bilgüvar K, Günel M, Başak A, Ertan S. FBXO7–R498X mutation: Phenotypic variability from chorea to early onset parkinsonism within a family. Parkinsonism & Related Disorders 2014, 20: 1253-1256. PMID: 25169713, DOI: 10.1016/j.parkreldis.2014.07.016.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentChoreaF-Box ProteinsFemaleHeterozygoteHomozygoteHumansMaleMutationParkinsonian DisordersPedigreePhenotypeConceptsEarly-onset parkinsonismPostural instabilityIndex caseFBXO7 mutationsPallido-pyramidal syndromeTremor-dominant parkinsonismIntrafamilial phenotypic variationDiverse clinical phenotypesMild parkinsonismClinical spectrumSevere apathyAtypical featuresParkinsonismOnset parkinsonismClinical phenotypeConsanguineous parentsMonogenic causesChoreaExomic sequencingSpeech problemsElder sisterGenetic findingsKurdish originPatientsMaternal grandfather
2013
Severe nigrostriatal degeneration without clinical parkinsonism in patients with polymerase gamma mutations
Tzoulis C, Tran G, Schwarzlmüller T, Specht K, Haugarvoll K, Balafkan N, Lilleng P, Miletic H, Biermann M, Bindoff L. Severe nigrostriatal degeneration without clinical parkinsonism in patients with polymerase gamma mutations. Brain 2013, 136: 2393-2404. PMID: 23625061, DOI: 10.1093/brain/awt103.Peer-Reviewed Original ResearchConceptsMitochondrial DNA abnormalitiesPolymerase gamma-encephalopathyCatalytic subunit of polymerase gammaMitochondrial diseaseCopy number of mitochondrial DNAMitochondrial DNA homeostasisDNA abnormalitiesMitochondrial quality controlPolymerase gamma mutationDopamine transporter imagingComplex I deficiencyLevels of deletionIn vivo functional studiesPositron emission tomographyPathogenesis of neurodegenerationMitochondrial DNADNA homeostasisSubstantia nigraPolymerase gammaCatalytic subunitNeurons of patientsRespiratory chainCopy numberClinical parkinsonismGamma mutations
2011
GPA protects the nigrostriatal dopamine system by enhancing mitochondrial function
Horvath TL, Erion DM, Elsworth JD, Roth RH, Shulman GI, Andrews ZB. GPA protects the nigrostriatal dopamine system by enhancing mitochondrial function. Neurobiology Of Disease 2011, 43: 152-162. PMID: 21406233, PMCID: PMC3623269, DOI: 10.1016/j.nbd.2011.03.005.Peer-Reviewed Original ResearchConceptsNormal chow-fed miceNigrostriatal dopamine systemChow-fed miceTH neuronsGuanidinopropionic acidNormal chowParkinson's diseaseDopamine systemMitochondrial functionMitochondrial dysfunctionModels of neurodegenerationMitochondrial numberAMPK activityMPTP treatmentMPTP intoxicationNigrostriatal functionNeuroprotective effectsMitochondrial respirationNeuroprotective propertiesStriatal dopamineAMPK-dependent increaseDisease progressionMouse modelMiceMPTP
2010
Dual-Radionuclide Brain SPECT for the Differential Diagnosis of Parkinsonism
El Fakhri G, Ouyang J. Dual-Radionuclide Brain SPECT for the Differential Diagnosis of Parkinsonism. Methods In Molecular Biology 2010, 680: 237-246. PMID: 21153385, DOI: 10.1007/978-1-60761-901-7_16.Peer-Reviewed Original ResearchConceptsDopamine transporter functionBrain SPECTDifferential diagnosis of parkinsonismDifferential diagnosisDiagnosis of parkinsonismIdiopathic Parkinson's diseaseDifferential diagnosis of idiopathic Parkinson’s diseaseDiagnosis of idiopathic Parkinson's diseaseCorticobasal degenerationProgressive supranuclear palsyParkinson's diseaseMultiple system atrophyParkinsonSPECT protocolCellular Repair in the Parkinsonian Nonhuman Primate Brain
Redmond DE, Weiss S, Elsworth JD, Roth RH, Wakeman DR, Bjugstad KB, Collier TJ, Blanchard BC, Teng YD, Synder EY, Sladek JR. Cellular Repair in the Parkinsonian Nonhuman Primate Brain. Rejuvenation Research 2010, 13: 188-194. PMID: 20370501, PMCID: PMC2946058, DOI: 10.1089/rej.2009.0960.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainDopamineEmbryonic Stem CellsHumansNerve RegenerationNeuronsParkinsonian DisordersPrimatesStem Cell TransplantationConceptsHuman neural stem cellsSubstantia nigraDopamine neuronsParkinson's diseaseFetal dopaminergic neuronsFetal striatal tissueReduction of medicationLittle therapeutic benefitParkinsonian motor deficitsSubsequent clinical trialsDopaminergic neural systemsNonhuman primate brainCell replacement strategiesLong-term improvementStem cellsNeural stem cellsMotor deficitsDopaminergic neuronsNeurological signsCellular repairClinical trialsStriatal targetsStriatal tissueTherapeutic benefitParkinson's patients
2008
Embryonic Stem Cell‐Derived Pitx3‐Enhanced Green Fluorescent Protein Midbrain Dopamine Neurons Survive Enrichment by Fluorescence‐Activated Cell Sorting and Function in an Animal Model of Parkinson's Disease
Hedlund E, Pruszak J, Lardaro T, Ludwig W, Viñuela A, Kim K, Isacson O. Embryonic Stem Cell‐Derived Pitx3‐Enhanced Green Fluorescent Protein Midbrain Dopamine Neurons Survive Enrichment by Fluorescence‐Activated Cell Sorting and Function in an Animal Model of Parkinson's Disease. Stem Cells 2008, 26: 1526-1536. PMID: 18388307, PMCID: PMC2693914, DOI: 10.1634/stemcells.2007-0996.Peer-Reviewed Original ResearchMeSH KeywordsAmphetamineAnimalsApomorphineCell DifferentiationCell SurvivalEmbryonic Stem CellsFlow CytometryGenes, ReporterGreen Fluorescent ProteinsHomeodomain ProteinsHydroxydopaminesMesencephalonMiceMitosisMotor ActivityParkinsonian DisordersRatsStem Cell TransplantationTranscription FactorsTransplantation, HeterologousConceptsFluorescence-activated cell sortingVesicular monoamine transporter 2Animal models of Parkinson's diseaseDopamine neuronsMidbrain dopamine neuronsModel of Parkinson's diseaseVentral mesencephalicAmino acid decarboxylaseTyrosine hydroxylaseAnimal modelsFetal ventral mesencephalicFetal VM cellsL-aromatic amino acid decarboxylaseEmbryonic stemES cellsMonoamine transporter 2Cell sortingParkinson's diseaseDifferentiation in vitroTreatment of Parkinson's diseaseProfile in vitroHost striatumDopaminergic populationIsolated neuronsMultiple cell types
2007
Rapid identification of disease‐causing mutations using copy number analysis within linkage intervals
Bayrakli F, Bilguvar K, Mason CE, DiLuna ML, Bayri Y, Gungor L, Terzi M, Mane SM, Lifton RP, State MW, Gunel M. Rapid identification of disease‐causing mutations using copy number analysis within linkage intervals. Human Mutation 2007, 28: 1236-1240. PMID: 17676595, DOI: 10.1002/humu.20592.Peer-Reviewed Original ResearchConceptsCopy number variationsComparative genome hybridization arraysParametric linkage analysisArray-based detectionCopy number analysisDisease-causing mutationsGenome rearrangementsLinkage intervalRapid identificationAutosomal recessive parkinsonismFunctional mutationsLinkage analysisNumber variationsRecessive parkinsonismHybridization arraysPARK2 geneReduced Neuron-Specific Expression of the TAF1 Gene Is Associated with X-Linked Dystonia-Parkinsonism
Makino S, Kaji R, Ando S, Tomizawa M, Yasuno K, Goto S, Matsumoto S, Tabuena M, Maranon E, Dantes M, Lee LV, Ogasawara K, Tooyama I, Akatsu H, Nishimura M, Tamiya. Reduced Neuron-Specific Expression of the TAF1 Gene Is Associated with X-Linked Dystonia-Parkinsonism. American Journal Of Human Genetics 2007, 80: 393-406. PMID: 17273961, PMCID: PMC1821114, DOI: 10.1086/512129.Peer-Reviewed Original ResearchMeSH KeywordsAdultAlu ElementsBlotting, NorthernCase-Control StudiesChromosomes, Human, XDNADown-RegulationDystoniaFemaleGenes, X-LinkedGenetic Diseases, X-LinkedHistone AcetyltransferasesHumansImmunoenzyme TechniquesMaleMiddle AgedMolecular Sequence DataNeuronsParkinsonian DisordersPedigreeRepetitive Sequences, Nucleic AcidReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTandem Repeat SequencesTATA BoxTATA-Binding Protein Associated FactorsTranscription Factor TFIIDConceptsNeuron-specific expressionDystonia-parkinsonismTAF1 geneDopamine receptor D2 geneMovement disordersCaudate nucleusBrain tissueDecreased expressionAbnormal patternsGenomic sequencing analysisFactor 1 geneExpression levelsCausative genesCaudateSVA retrotransposon insertionD2 geneSequencing analysis
2005
Uncoupling Protein-2 Is Critical for Nigral Dopamine Cell Survival in a Mouse Model of Parkinson's Disease
Andrews ZB, Horvath B, Barnstable CJ, Elseworth J, Yang L, Beal MF, Roth RH, Matthews RT, Horvath TL. Uncoupling Protein-2 Is Critical for Nigral Dopamine Cell Survival in a Mouse Model of Parkinson's Disease. Journal Of Neuroscience 2005, 25: 184-191. PMID: 15634780, PMCID: PMC6725213, DOI: 10.1523/jneurosci.4269-04.2005.Peer-Reviewed Original ResearchMeSH Keywords1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine1-Methyl-4-phenylpyridiniumAnimalsCell SurvivalCorpus StriatumDisease Models, AnimalDopamineHumansImmunohistochemistryIon ChannelsMaleMembrane Transport ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMitochondriaMitochondrial ProteinsOxygen ConsumptionParkinsonian DisordersReactive Oxygen SpeciesSubstantia NigraUncoupling Protein 2ConceptsProtein 2Mitochondrial ROS productionLack of UCP2Reactive oxygen species productionGenetic manipulationOxygen species productionMitochondria numberCell metabolismATP synthesisCell survivalOverexpression of UCP2Wild-type controlsMitochondrial uncouplingNovel therapeutic targetROS productionUCP2Species productionElectron microscopic analysisOverexpressionCell functionUCP2 overexpressionDopamine cell survivalTherapeutic targetFluorescent ethidiumDopamine cell function
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