Search results for "synuclein"

showing 10 items of 42 documents

Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by alpha-synuclein.

2010

Although generally considered a prototypical movement disorder, Parkinson's disease is commonly associated with a broad-spectrum of non-motor symptoms, including autonomic dysfunctions caused by significant alterations in catecholaminergic neurons of the peripheral sympathetic nervous system. Here we present evidence that alpha-synuclein is highly expressed by sympathetic ganglion neurons throughout embryonic and postnatal life and that it is found in tyrosine hydroxylase-positive sympathetic fibers innervating the heart of adult mice. However, mice deficient in alpha-synuclein do not exhibit any apparent alterations in sympathetic development. Sympathetic neurons isolated from mouse embryo…

Sympathetic nervous system1-Methyl-4-phenylpyridiniumα-Synuclein knockoutTyrosine 3-MonooxygenaseNeurotoxinsNeurotrophic factorSubstantia nigraBiologylcsh:RC321-571chemistry.chemical_compoundMiceCatecholaminesSympathetic Fibers PostganglionicParkinsonian DisordersNeurotrophic factorsmedicineNeurotoxinAutonomic gangliaAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCells CulturedNeuronsGanglia SympatheticCell DeathMPTPSympathetic ganglionMice Mutant Strainsnervous system diseasesMPP+medicine.anatomical_structureNeurologychemistrynervous system1-Methyl-4-phenyl-1236-tetrahydropyridinePeripheral nervous systemSympathetic nervous systemNerve Degenerationalpha-SynucleinCatecholaminergic cell groupsPeripheral nervous systemNeuroscienceNeurobiology of disease
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Knowledge-based modelling applied to synucleinopathies

2015

International audience; The adoption of telemedicine technologies has enabled collaborative programs involving a variety of links among distributed medical structures and health officials and professionals. The use for telemedicine for transmission of medical data and the possibility for several distant physicians to share their knowledge on given medical cases provides clear benefits, but also raises several unsolved conceptual and technical challenges. The seamless exchange and access of medical information between medical structures, health professionals, and patients is a prerequisite for the harmonious development of this new medical practice. This paper proposes a new approach of sema…

Telemedicine[ INFO.INFO-MO ] Computer Science [cs]/Modeling and SimulationKnowledge managementOntological knowledgeContext (language use)02 engineering and technologyDisease[ SDV.MHEP.GEG ] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologySemantic modelling03 medical and health sciences0302 clinical medicine0202 electrical engineering electronic engineering information engineeringMedicineMedical diagnosisSynucleinopathiesbusiness.industry[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologySemantic interoperabilityModélisation et simulation[INFO.INFO-MO]Computer Science [cs]/Modeling and SimulationCollaborationTelemedicine3. Good healthVariety (cybernetics)GeriatricsConceptual graphGériatrie et gérontologie020201 artificial intelligence & image processingGeriatrics and GerontologybusinessGerontology030217 neurology & neurosurgery
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α-Synuclein expression levels do not significantly affect proteasome function and expression in mice and stably transfected PC12 cell lines

2004

α-Synuclein (α-syn) is a small protein of unknown function that is found aggregated in Lewy bodies, the histopathological hallmark of sporadic Parkinson disease and other synucleinopathies. Mutations in the α-syn gene and a triplication of its gene locus have been identified in early onset familial Parkinson disease. α-Syn turnover can be mediated by the proteasome pathway. A survey of published data may lead to the suggestion that overexpression of α-syn wild type, and/or their variants (A53T and A30P), may produce a decrease in proteasome activity and function, contributing to α-syn aggregation. To investigate the relationship between synuclein expression and proteasome function we have s…

Time Factorsanimal diseasesmedicine.disease_causePC12 CellsBiochemistryMicechemistry.chemical_compoundTransgenesPromoter Regions GeneticMice KnockoutGeneticsMutationInnervationBrainParkinson DiseaseProteasome complexAmyloidosisCell biologyInnervacióalpha-SynucleinAdditions and CorrectionsPèptidsPlasmidsProteasome Endopeptidase ComplexPrionsProtein subunitBlotting WesternImmunoblottingSynucleinsMice TransgenicNerve Tissue ProteinsBiologyTransfectionBacterial ProteinsMultienzyme ComplexesmedicineAnimalsImmunoprecipitationMolecular BiologyAlpha-synucleinSynucleinopathiesEpilepsyWild typeGenetic VariationCell BiologyAxonsRatsnervous system diseasesMice Inbred C57BLEpilèpsiaDisease Models AnimalLuminescent ProteinschemistryProteasomenervous systemSinapsiMutationSynapsesSynucleinAmiloïdosiPeptides
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Microglia and α-synuclein implication in Parkinson's disease

2011

Age-related neurodegenerative disorders like Parkinson’s disease take an enormous toll on individuals and on society. Despite extensive efforts, Parkinson’s disease remains incurable and only very limited treatments exist. Indeed, Parkinson’s pathogenesis is still not clear and research on its molecular mechanisms is ongoing. In this study, we focused our interest on two abnormal events occurring in Parkinson’s patients, namely α-synuclein aggregation and microglial activation. We first investigated α-synuclein and its abnormal polymerisation. For this purpose, we developed novel methods, which allowed the in vitro production of different types of α-synuclein oligomers. Using highly sensiti…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciencesΑ-synucléineAgingMaladie de ParkinsonDopamineCultures primairesBrain immunityNeuronesVieillissementImmunité du cerveauPotassium channelsNeuroinflammationToxicitéC8-B4 cell line[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMéthode d’isolation in vitroElectrophysiologieCanaux potassiquesNeurodegeneration[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciencesIn vitro isolation methodPrimary cultureKv1.3 - Kir2.1Neurons[SDV.SA] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyToxicityMaladies neurodégénérativesΑ-synucleinNitric oxideNeurodégénérationOligomèresElectrophysiologyMicrogliesBrain macrophagesOligomersOxyde nitriqueNeurodegenerative disordersParkinson’s diseaseCytokinesLignée cellulaire C8-B4MicrogliaPatch-clamp[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Focus on the Small GTPase Rab1: A Key Player in the Pathogenesis of Parkinson’s Disease

2021

Parkinson’s disease (PD) is the second most frequent neurodegenerative disease. It is characterized by the loss of dopaminergic neurons in the substantia nigra and the formation of large aggregates in the survival neurons called Lewy bodies, which mainly contain α-synuclein (α-syn). The cause of cell death is not known but could be due to mitochondrial dysfunction, protein homeostasis failure, and alterations in the secretory/endolysosomal/autophagic pathways. Survival nigral neurons overexpress the small GTPase Rab1. This protein is considered a housekeeping Rab that is necessary to support the secretory pathway, the maintenance of the Golgi complex structure, and the regulation of macroau…

autophagyParkinson's diseaseQH301-705.5Substantia nigraReviewBiologyCatalysisInorganic Chemistryα-synucleinmedicineAnimalsHumansSmall GTPaseBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopySecretory pathwayRab1GTPasesOrganic ChemistryNeurodegenerationDopaminergicRAB1Parkinson DiseaseLRRK2General Medicinemedicine.diseaseLRRK2Computer Science Applicationssecretory pathwayrab1 GTP-Binding ProteinsChemistrynervous systemParkinson’s diseaseNeuroscienceGolgi fragmentationInternational Journal of Molecular Sciences
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Formation of covalent di-tyrosine dimers in recombinant α-synuclein

2015

Parkinson's disease is associated with fibril deposition in the diseased brain. Misfolding events of the intrinsically disordered synaptic protein α-synuclein are suggested to lead to the formation of transient oligomeric and cytotoxic species. The etiology of Parkinson's disease is further associated with mitochondrial dysfunction and formation of reactive oxygen species. Oxidative stress causes chemical modification of native α-synuclein, plausibly further influencing misfolding events. Here, we present evidence for the spontaneous formation of covalent di-tyrosine α-synuclein dimers in standard recombinant protein preparations, induced without extrinsic oxidative or nitrative agents. The…

chemistry.chemical_classificationReactive oxygen speciesParkinson's diseasealphasynucleinamyloids di-tyrosine dimers EOM Parkinson’s disease SAXSSAXSOxidative phosphorylationFibrilmedicine.disease_causeIndustrial and Manufacturing Engineeringchemistry.chemical_compoundα-synucleinMonomerchemistryBiochemistryCovalent bondmedicinedi-tyrosine dimersamyloidsTyrosineProtein secondary structureEOMOxidative stressResearch PaperIntrinsically Disordered Proteins
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Fabry Disease With Concomitant Lewy Body Disease

2019

AbstractAlthough Gaucher disease can be accompanied by Lewy pathology (LP) and extrapyramidal symptoms, it is unknown if LP exists in Fabry disease (FD), another progressive multisystem lysosomal storage disorder. We aimed to elucidate the distribution patterns of FD-related inclusions and LP in the brain of a 58-year-old cognitively unimpaired male FD patient suffering from predominant hypokinesia. Immunohistochemistry (CD77, α-synuclein, collagen IV) and neuropathological staging were performed on 100-µm sections. Tissue from the enteric or peripheral nervous system was unavailable. As controls, a second cognitively unimpaired 50-year-old male FD patient without LP or motor symptoms and 3…

complications [Lewy Body Disease]MalePathologyAutopsyDisease0302 clinical medicineHypokinesiapathology [Brain]Lysosomal storage diseasespathology [Neurons]metabolism [alpha-Synuclein]metabolism [Fabry Disease]pathology [Astrocytes]Neuronsα-Synuclein0303 health sciencesParkinsonismTrihexosylceramidesBrainGeneral MedicineMiddle AgedParkinson diseasecomplications [Fabry Disease]Neurologymetabolism [Neurons]alpha-Synucleinmedicine.symptomLewy Body Diseasemedicine.medical_specialtymetabolism [Lewy Body Disease]Context (language use)Substantia nigrametabolism [Trihexosylceramides]Pathology and Forensic Medicineblood supply [Brain]03 medical and health sciencesCellular and Molecular Neuroscienceα-Galactosidase AmedicineHumansddc:610030304 developmental biologypathology [Lewy Bodies]Fabry diseasebusiness.industryPars compactapathology [Lewy Body Disease]Lewy bodies/neuritesOriginal Articlesmetabolism [Lewy Bodies]medicine.diseaseFabry diseasemetabolism [Brain]AstrocytesLewy BodiesNeurology (clinical)CD77pathology [Fabry Disease]business030217 neurology & neurosurgeryJournal of Neuropathology and Experimental Neurology
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Reductive modification of genetically encoded 3-nitrotyrosine sites in alpha synuclein expressed in E.coli

2019

Tyrosine nitration is a post-translational protein modification relevant to various pathophysiological processes. Chemical nitration procedures have been used to generate and study nitrated proteins, but these methods regularly lead to modifications at other amino acid residues. A novel strategy employs a genetic code modification that allows incorporation of 3-nitrotyrosine (3-NT) during ribosomal protein synthesis to generate a recombinant protein with defined 3-NT-sites, in the absence of other post-translational modifications. This approach was applied to study the generation and stability of the 3-NT moiety in recombinant proteins produced in E.coli. Nitrated alpha-synuclein (ASYN) was…

lcsh:R5-920Escherichia coli ProteinsGenetic VectorsGreen Fluorescent ProteinsGene ExpressionProtein EngineeringRecombinant Proteinslcsh:Biology (General)ddc:570Escherichia colialpha-SynucleinHumansTyrosineCloning MolecularAlpha synuclein Nitration 3-Nitrotyrosine 3-Aminotyrosine E.colilcsh:Medicine (General)Oxidation-Reductionlcsh:QH301-705.5Metabolic Networks and PathwaysResearch Paper
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Perivascular nerve fiber α-synuclein regulates contractility of mouse aorta: A link to autonomic dysfunction in Parkinson's disease

2010

Parkinson's disease and other neurodegenerative disorders associated to changes in alpha-synuclein often result in autonomic dysfunction, most of the time accompanied by abundant expression of this synaptic protein in peripheral autonomic neurons. Given that expression of alpha-synuclein in vascular elements has been previously reported, the present study was undertaken to determine whether alpha-synuclein directly participates in the regulation of vascular responsiveness. We detected by immunohistochemistry perivascular nerve fibers containing alpha-synuclein in the aorta of mice while aortic endothelial cells and muscular fibers themselves did not exhibit detectable levels of this protein…

medicine.medical_specialtyPresynaptic TerminalsAorta ThoracicVasodilationBiologyMuscle Smooth VascularMiceCellular and Molecular Neurosciencechemistry.chemical_compoundSympathetic Fibers PostganglionicDopaminemedicine.arteryInternal medicinemedicineAnimalsNeurotransmitterMice KnockoutAortaEndothelial CellsParkinson DiseaseCell Biologynervous system diseasesMice Inbred C57BLEndocrinologyAutonomic Nervous System Diseasesnervous systemchemistryVasoconstrictionKnockout mousealpha-SynucleinCatecholaminemedicine.symptomVasoconstrictionAcetylcholineMuscle Contractionmedicine.drugNeurochemistry International
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Prosurvival effect of human wild-type alpha-synuclein on MPTP-induced toxicity to central but not peripheral catecholaminergic neurons isolated from …

2010

In the present work we report the generation of a new line of alpha-synuclein (alpha-SYN) transgenic mice in which the human wild-type alpha-SYN cDNA is expressed under the control of a tyrosine hydroxylase (TH) promoter. We provide evidence that the ectopic protein is found in TH expressing neurons of both central and peripheral nervous systems. The transgene is expressed very early in development coinciding with the activity of the TH promoter and in the adult brain the human protein distributes normally to the nerve endings and cell bodies of dopaminergic nigral neurons without any evidence of abnormal aggregation. Our results indicate that expression of human wild-type alpha-SYN does no…

medicine.medical_specialtySympathetic Nervous SystemTyrosine 3-MonooxygenaseTransgeneMice Transgenicchemistry.chemical_compoundMiceCatecholaminesDopamineMesencephalonInternal medicinemedicineNeurotoxinAnimalsHumansTransgenesPromoter Regions GeneticCells CulturedDopamine transporterNeuronsDopamine Plasma Membrane Transport ProteinsTyrosine hydroxylasebiologyCell DeathGeneral NeuroscienceMPTPDopaminergicBrainEndocrinologynervous systemchemistry1-Methyl-4-phenyl-1236-tetrahydropyridineOrgan Specificitybiology.proteinalpha-SynucleinCatecholaminergic cell groupsmedicine.drugNeuroscience
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