Search results for "neurotrophin"

showing 10 items of 83 documents

Targeting Alzheimer’s disease with multimodal polypeptide-based nanoconjugates

2021

LRP1-targeted St-Cl–polyglutamate conjugates as multivalent neuroprotective/neurotrophic therapeutics for Alzheimer’s disease.

Alzheimer’s disease (AD)Mice TransgenicNanoconjugatesHippocampal formationHippocampusNeuroprotectionAD treatmentMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAlzheimer DiseaseBisdemethoxycurcuminAnimalsOlfactory memoryResearch Articles030304 developmental biology0303 health sciencesAmyloid beta-PeptidesMultidisciplinaryPolyglutamatebiologySciAdv r-articlesLife Sciences3. Good healthOlfactory bulbDisease Models AnimalApplied Sciences and Engineeringchemistrybiology.proteinNeuroscience030217 neurology & neurosurgeryNanoconjugatesResearch ArticleNeurotrophinScience Advances
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88 SYNAPTIC SECRETION AND LOCAL ACTIONS OF NEUROTROPHINS

2007

Anesthesiology and Pain Medicinebiologybiology.proteinSecretionNeuroscienceNeurotrophinEuropean Journal of Pain
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4

2015

A body of experimental evidence suggests that T cells mediate neuroprotection following CNS injury; however, the antigen specificity of these T cells and how they mediate neuroprotection are unknown. Here, we have provided evidence that T cell-mediated neuroprotection after CNS injury can occur independently of major histocompatibility class II (MHCII) signaling to T cell receptors (TCRs). Using two murine models of CNS injury, we determined that damage-associated molecular mediators that originate from injured CNS tissue induce a population of neuroprotective, IL-4-producing T cells in an antigen-independent fashion. Compared with wild-type mice, IL-4-deficient animals had decreased functi…

CD4-Positive T-LymphocytesCancer ResearchMAP Kinase Signaling SystemPopulationReceptors Antigen T-CellInflammationBiologyNeuroprotectionMiceAntigenClinical investigationAnimalsMedicineExtracellular Signal-Regulated MAP KinaseseducationReceptorInterleukin 4Mice Knockouteducation.field_of_studybusiness.industryT-cell receptorHistocompatibility Antigens Class IINeurodegenerative DiseasesGeneral MedicineAxonsCell biologyBrain InjuriesMyeloid Differentiation Factor 88Immunologybiology.proteinInterleukin-4medicine.symptomFunction and Dysfunction of the Nervous SystemCorrigendumbusinessProto-Oncogene Proteins c-aktResearch ArticleNeurotrophinJournal of Clinical Investigation
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Postsynaptic Secretion of BDNF and NT-3 from Hippocampal Neurons Depends on Calcium–Calmodulin Kinase II Signaling and Proceeds via Delayed Fusion Po…

2007

The mammalian neurotrophins (NTs) NGF, BDNF, NT-3, and NT-4 constitute a family of secreted neuronal growth factors. In addition, NTs are implicated in several forms of activity-dependent synaptic plasticity. Although synaptic secretion of NTs has been described, the intracellular signaling cascades that regulate synaptic secretion of NTs are far from being understood. Analysis of NT secretion at the subcellular level is thus required to resolve the role of presynaptic and postsynaptic NT secretion for synaptic plasticity. Here, we transfected cultures of dissociated rat hippocampal neurons with green fluorescent protein-tagged versions of BDNF and NT-3, respectively, and identified NT vesi…

Calcium Channels L-TypeBiologyNeurotransmissionInhibitory postsynaptic potentialHippocampusReceptors N-Methyl-D-AspartateSynaptic TransmissionExocytosisNeurotrophin 3Postsynaptic potentialCa2+/calmodulin-dependent protein kinaseAnimalsCalcium SignalingNeuronsBrain-Derived Neurotrophic FactorGeneral NeuroscienceRyanodine Receptor Calcium Release ChannelLong-term potentiationArticlesCyclic AMP-Dependent Protein KinasesRatsCell biologynervous systemBiochemistryTrk receptorCalcium-Calmodulin-Dependent Protein KinasesSynapsesSynaptic plasticityThapsigarginCalcium-Calmodulin-Dependent Protein Kinase Type 2Postsynaptic densityThe Journal of Neuroscience
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Central nicotinic receptors, neurotrophic factors and neuroprotection

2000

The multiple combinations of nAChR subunits identified in central nervous structures possess distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely ind…

Cell SurvivalAgonist-antagonistCentral nervous systemReceptors Nicotiniccomplex mixturesNeuroprotectionBehavioral NeuroscienceNeurotrophic factorsmental disordersmedicineAnimalsHumansNerve Growth FactorsAcetylcholine receptorNeuronsRegulation of gene expressionbiologymusculoskeletal neural and ocular physiologyBrainHaplorhinimedicine.diseaseRatsNeuroprotective Agentsmedicine.anatomical_structurenervous systembiology.proteinFibroblast Growth Factor 2sense organsAlzheimer's diseasePsychologyNeuroscienceNeurotrophinBehavioural Brain Research
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Brain and Cancer: The Protective Role of Erythropoietin

2005

Erythropoietin (Epo) is a pleiotropic agent, that is to say, it can act on several cell types in different ways. An independent system Epo/Epo receptor (EpoR) was detected in brain, leading to the hypothesis that this hormone could be involved in cerebral functions. Epo/EpoR expression changes during ontogenesis, thus indicating the importance of this system in neurodevelopment. Moreover, the hypoxia-induced production of Epo in the adult brain suggests that it could exert a neurotrophic and neuroprotective effect in case of brain injury. Epo could also influence neuro- transmission, inducing neurotransmitters (NT) release. Epo therapy in anemic cancer patients is still a controversial issu…

Cell typeCentral nervous systemPharmacologyModels BiologicalNeuroprotectionNeoplasmshemic and lymphatic diseasesDrug DiscoveryReceptors ErythropoietinmedicineAnimalsHumanscancerReceptorPleiotropyPharmacologyNeurotransmitter AgentsNeovascularization Pathologicbiologyhypoxiabusiness.industryMedicine (all)Organic ChemistryBrainangiogenesiGeneral MedicineNeuroprotectionneuroprotective effectErythropoietin receptorErythropoietin (Epo); brain; central nervous system (CNS) diseases; neuroprotective effectmedicine.anatomical_structureErythropoietin (Epo)Erythropoietinbiology.proteinMolecular MedicineerythropoietinSignal transductionbusinessNeurosciencecentral nervous system (CNS) diseasesmedicine.drugNeurotrophinChemInform
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Neurotrophin secretion: current facts and future prospects

2003

The proteins of the mammalian neurotrophin family (nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4/5)) were originally identified as neuronal survival factors. During the last decade, evidence has accumulated implicating them (especially BDNF) in addition in the regulation of synaptic transmission and synaptogenesis in the CNS. However, a detailed understanding of the secretion of neurotrophins from neurons is required to delineate their role in regulating synaptic function. Some crucial questions that need to be addressed include the sites of neurotrophin secretion (i.e. axonal versus dendritic; synaptic versus extrasyna…

Central Nervous SystemNeuronsNeuronal PlasticityArc (protein)biologyCell SurvivalGeneral NeuroscienceSynaptogenesisLong-term potentiationAMPA receptorNeurotransmissionCell Linenervous systemNeurotrophic factorsTrk receptorbiology.proteinAnimalsHumansNerve Growth FactorsPeptidesNeuroscienceForecastingNeurotrophinProgress in Neurobiology
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Effects of escitalopram on the regulation of brain-derived neurotrophic factor and nerve growth factor protein levels in a rat model of chronic stres…

2009

Escitalopram (ES-CIT) is a widely used, highly specific antidepressant. Until now there has been very little evidence on how this drug under pathological conditions affects an important feature within the pathophysiology of stress-related disorders such as depression: the endogenous neurotrophins. By using a well-characterized rat model in which chronic stress induces depressive-like behavior, the levels of neurotrophins brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were determined in representative brain regions and serum using a highly sensitive improved fluorometric two-site ELISA system. There was a significant increase of BDNF in the left and right cortices aft…

Dominance-SubordinationMalemedicine.medical_specialtyDrinking BehaviorEnzyme-Linked Immunosorbent AssayCitalopramFunctional LateralityCellular and Molecular NeuroscienceNeurotrophic factorsInternal medicineAdrenal GlandsNerve Growth FactormedicineAnimalsChronic stressRats WistarSocial stressBrain-derived neurotrophic factorbiologyBrain-Derived Neurotrophic FactorBody WeightBrainOrgan SizeCortex (botany)RatsEndocrinologyNerve growth factornervous systemChronic Diseasebiology.proteinLinear ModelsAntidepressantAntidepressive Agents Second-GenerationPsychologyStress PsychologicalNeurotrophinJournal of neuroscience research
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Neuromuscular junction disassembly and muscle fatigue in mice lacking neurotrophin-4

2001

Neurotrophin-4 (NT-4) is produced by slow muscle fibers in an activity-dependent manner and promotes growth and remodeling of adult motorneuron innervation. However, both muscle fibers and motor neurons express NT-4 receptors, suggesting bidirectional NT-4 signaling at the neuromuscular junction. Mice lacking NT-4 displayed enlarged and fragmented neuromuscular junctions with disassembled postsynaptic acetylcholine receptor (AChR) clusters, reduced AChR binding, and acetylcholinesterase activity. Electromyographic responses, posttetanic potentiation, and action potential amplitude were also significantly reduced in muscle fibers from NT-4 knock-out mice. Slow-twitch soleus muscles from thes…

End-plate potentialNeuromuscular JunctionElectromyographyBiologyNeuromuscular junctionCellular and Molecular NeuroscienceMicePostsynaptic potentialmedicineAnimalsReceptors CholinergicNerve Growth FactorsMuscle SkeletalMolecular BiologyAcetylcholine receptorMice KnockoutMotor Neuronsmedicine.diagnostic_testMuscle fatigueElectromyographyAge FactorsLong-term potentiationneuromuscular junction; neurotrophin-4; synaptic transmissionCell Biologymedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle FatigueAcetylcholinesteraseTetanic stimulationNeuroscienceMuscle Contraction
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