Search results for "DEGENERATION"

showing 10 items of 601 documents

Identification of potential therapeutic compounds for Parkinson's disease using Drosophila and human cell models.

2017

Abstract Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease. It is caused by a loss of dopaminergic neurons in the substantia nigra pars compacta, leading to a decrease in dopamine levels in the striatum and thus producing movement impairment. Major physiological causes of neurodegeneration in PD are oxidative stress (OS) and mitochondrial dysfunction; these pathophysiological changes can be caused by both genetic and environmental factors. Although most PD cases are sporadic, it has been shown that 5–10% of them are familial forms caused by mutations in certain genes. One of these genes is the DJ-1 oncogene, which is involved in an early…

0301 basic medicineParkinson's diseaseProtein Deglycase DJ-1Drug Evaluation PreclinicalSubstantia nigraNerve Tissue ProteinsBiologymedicine.disease_causeBiochemistryAnimals Genetically Modified03 medical and health sciences0302 clinical medicineDopaminePhysiology (medical)Cell Line TumorDrug DiscoverymedicineAnimalsDrosophila ProteinsHumansGeneticsMutationPars compactaNeurodegenerationDopaminergicParkinson Diseasemedicine.diseaseDisease Models AnimalOxidative Stress030104 developmental biologyGene Knockdown TechniquesMutationCancer researchDrosophila030217 neurology & neurosurgeryOxidative stressLocomotionmedicine.drugFree radical biologymedicine
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A longitudinal DTI and histological study of the spinal cord reveals early pathological alterations in G93A-SOD1 mouse model of amyotrophic lateral s…

2017

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective motor neuron degeneration in the motor cortex, brainstem and spinal cord. It is generally accepted that ALS is caused by death of motor neurons, however the exact temporal cascade of degenerative processes is not yet completely known. To identify the early pathological changes in spinal cord of G93A-SOD1 AIS mice we performed a comprehensive longitudinal analysis employing diffusion-tensor magnetic resonance imaging alongside histology and electron microscopy, in parallel with peripheral nerve histology. We showed the gradient of degeneration appearance in spinal cord white and gray matter, startin…

0301 basic medicinePathologyNeurologyTime FactorsMotor neuron diseasesSensory Receptor CellMice0302 clinical medicineImage Processing Computer-AssistedAxonAmyotrophic lateral sclerosisGray MatterAnthracenesWhite MatterMitochondriamedicine.anatomical_structureDiffusion Tensor ImagingNeurologySpinal CordG93A-SOD1 miceBrainstemHumanMotor cortexmedicine.medical_specialtyAxon degenerationTime FactorSensory Receptor CellsSOD1Mice TransgenicWhite matter03 medical and health sciencesMagnetic resonance imagingDevelopmental NeuroscienceMicroscopy Electron TransmissionmedicineElectron microscopyAnimalsHumansMotor neuron diseaseAmyotrophic lateral sclerosiAnimalbusiness.industrySuperoxide DismutaseAmyotrophic Lateral SclerosisSpinal cordmedicine.diseaseAmyotrophic lateral sclerosisMice Inbred C57BLDisease Models Animal030104 developmental biologyAnthracenebusinessNeuroscience030217 neurology & neurosurgeryExperimental neurology
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Irreversible changes occurring in long-term denervated Schwann cells affect delayed nerve repair.

2017

OBJECTIVEMultiple factors may affect functional recovery after peripheral nerve injury, among them the lesion site and the interval between the injury and the surgical repair. When the nerve segment distal to the lesion site undergoes chronic degeneration, the ensuing regeneration (when allowed) is often poor. The aims of the current study were as follows: 1) to examine the expression changes of the neuregulin 1/ErbB system during long-term nerve degeneration; and 2) to investigate whether a chronically denervated distal nerve stump can sustain nerve regeneration of freshly axotomized axons.METHODSThis study used a rat surgical model of delayed nerve repair consisting of a cross suture betw…

0301 basic medicinePathologymedicine.medical_specialtyTime FactorsNerve rootNeuregulin-1Settore MED/19 - Chirurgia PlasticaSchwann cellNRG1/ErbB system03 medical and health sciences0302 clinical medicinePeripheral Nerve InjuriesMedicineAnimalsNeuregulin 1Rats Wistardelayed nerve repairDenervationneuregulin 1biologybusiness.industryRegeneration (biology)General MedicineAnatomyRecovery of FunctionDenervationMedian nerveNerve RegenerationRats030104 developmental biologymedicine.anatomical_structureperipheral nervePeripheral nerve injuryNerve Degenerationstereologybiology.proteinFemaleSchwann CellsbusinessEpineurial repair030217 neurology & neurosurgeryJournal of neurosurgery
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Activation of microglia synergistically enhances neurodegeneration caused by MPP+ in human SH-SY5Y cells

2019

While MPP+ may not directly activate microglia, the initial neuronal damage inflicted by the toxin may trigger microglia, possibly leading to synergistic pro-apoptotic interaction between neuro-inflammation and toxin-induced neurotoxicity, which may further aggravate neurodegeneration. However, what molecular targets are synergistically up or downregulated during this interaction is not well understood. Here, we addressed this by co-culturing fully differentiated human SH-SY5Y cells treated with parkinsonian toxin 1-Methyl-4-phenylpyridinium (MPP+), with endotoxin-activated microglial cell line EOC 20 to determine how this interaction affects pro-apoptotic (p38, JNK, and bax:bcl2 ratios) an…

0301 basic medicinePharmacologySH-SY5YMicrogliaChemistryp38 mitogen-activated protein kinasesNeurodegenerationNeurotoxicityInflammationmedicine.diseaseCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureApoptosismedicineViability assaymedicine.symptom030217 neurology & neurosurgeryEuropean Journal of Pharmacology
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Effects of air pollution particles (ultrafine and fine particulate matter) on mitochondrial function and oxidative stress – Implications for cardiova…

2020

Environmental pollution is a major cause of global mortality and burden of disease. All chemical pollution forms together may be responsible for up to 12 million annual excess deaths as estimated by the Lancet Commission on pollution and health as well as the World Health Organization. Ambient air pollution by particulate matter (PM) and ozone was found to be associated with an all-cause mortality rate of up to 9 million in the year 2015, with the majority being of cerebro- and cardiovascular nature (e.g. stroke and ischemic heart disease). Recent evidence suggests that exposure to airborne particles and gases contributes to and accelerates neurodegenerative diseases. Especially, airborne t…

0301 basic medicinePollutionmedia_common.quotation_subjectBiophysicsAir pollutionEnvironmental pollutionDiseasemedicine.disease_causeBiochemistry03 medical and health sciencesEnvironmental healthMedicineAnimalsHumansEnvironmental risk factorsNeurodegenerationMolecular Biologymedia_commonMitochondrial damage and dysfunctionAir Pollutants030102 biochemistry & molecular biologybusiness.industryMortality rateNeurodegenerationNeurodegenerative DiseasesParticulatesmedicine.diseaseCardiovascular diseaseMitochondriaOxidative Stress030104 developmental biologyCardiovascular DiseasesAmbient air pollution; Cardiovascular disease; Environmental risk factors; Mitochondrial damage and dysfunction; Neurodegeneration; Particulate matter; Air Pollutants; Animals; Cardiovascular Diseases; Humans; Mitochondria; Neurodegenerative Diseases; Oxidative Stress; Particulate MatterParticulate MatterAmbient air pollutionbusinessOxidative stress
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How Can Interleukin-1 Receptor Antagonist Modulate Distinct Cell Death Pathways?

2018

Multiple mechanisms of cell death exist (apoptosis, necroptosis, pyroptosis) and the subtle balance of several distinct proteins and inhibitors tightly regulates the cell fate toward one or the other pathway. Here, by combining coimmunoprecipitation, enzyme assays, and molecular simulations, we ascribe a new role, within this entangled regulatory network, to the interleukin-1 receptor antagonist (IL-1Ra). Our study enlightens that IL-1Ra, which usually inhibits the inflammatory effects of IL-1α/β by binding to IL-1 receptor, under advanced pathological states prevents apoptosis and/or necroptosis by noncompetitively inhibiting the activity of caspase-8 and -9. Consensus docking, followed by…

0301 basic medicineProgrammed cell deathProtein ConformationGeneral Chemical EngineeringNecroptosis-Library and Information SciencesMolecular Dynamics SimulationInhibitor of apoptosis01 natural sciencesArticle03 medical and health sciences0103 physical sciencesReceptorsmedicineCaspaseCaspase 8010304 chemical physicsbiologyCell DeathChemistryNeurodegenerationPyroptosisComputational BiologyReceptors Interleukin-1General Chemistrymedicine.diseaseCaspase 9Computer Science ApplicationsCell biologyXIAPEnzyme ActivationInterleukin 1 Receptor Antagonist Protein030104 developmental biologyApoptosisbiology.proteinThermodynamicsInterleukin-1
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1

2021

Contains fulltext : 232759.pdf (Publisher’s version ) (Closed access) In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to…

0301 basic medicineProgrammed cell deathSettore BIO/06AutophagosomeAutolysosome[SDV]Life Sciences [q-bio]lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Autophagy-Related ProteinsReviewComputational biology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologySettore MED/0403 medical and health sciencesstressChaperone-mediated autophagyddc:570AutophagyLC3AnimalsHumanscancerSettore BIO/10Autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSet (psychology)Molecular Biologyvacuole.phagophore030102 biochemistry & molecular biologyvacuolebusiness.industryInterpretation (philosophy)AutophagyAutophagosomesneurodegenerationCell BiologyfluxMulticellular organismmacroautophagy030104 developmental biologyKnowledge baselysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleBiological AssayLysosomesbusinessBiomarkers[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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The endoplasmic reticulum unfolded protein response in neurodegenerative disorders and its potential therapeutic significance

2017

In eukaryotic cells, the endoplasmic reticulum (ER) is the cell compartment involved in secretory protein translocation and quality control of secretory protein folding. Different conditions can alter ER function, resulting in the accumulation of unfolded or misfolded proteins within the ER lumen. Such a condition, known as ER stress, elicits an integrated adaptive response known as the unfolded protein response (UPR) that aims to restore proteostasis within the secretory pathway. Conversely, in prolonged cell stress or insufficient adaptive response, UPR signaling causes cell death. ER dysfunctions are involved and contribute to neuronal degeneration in several human diseases, including Al…

0301 basic medicineProgrammed cell deathTherapeutic targetReviewBiologytherapeutic targetsNeurodegenerative diseaselcsh:RC321-571Unfolded protein response03 medical and health sciencesCellular and Molecular NeuroscienceProtein misfolding disordermedicineneurodegenerative diseasesprotein misfolding disorderslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologySecretory pathwayEndoplasmic reticulumNeurodegenerationmedicine.diseaseCell biology030104 developmental biologyProteostasisSecretory proteinUnfolded protein responseER streSignal transductionER stressNeuroscience
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Breaking BAG: The Co-Chaperone BAG3 in Health and Disease.

2016

Human BAG ( B cl-2-associated a thano g ene) proteins form a family of antiapoptotic proteins that currently consists of six members (BAG1–6) all sharing the BAG protein domain from which the name arises. Via this domain, BAG proteins bind to the heat shock protein 70 (Hsp70), thereby acting as a co-chaperone regulating the activity of Hsp70. In addition to their antiapoptotic activity, all human BAG proteins have distinct functions in health and disease, and BAG3 in particular is the focus of many investigations. BAG3 has a modular protein domain composition offering the possibility for manifold interactions with other proteins. Various BAG3 functions are implicated in disorders including …

0301 basic medicineProtein domainCellular homeostasisBiologyToxicologyBAG303 medical and health sciencesMuscular DiseasesNeoplasmsmedicineAutophagyAnimalsHumansHSP70 Heat-Shock ProteinsAdaptor Proteins Signal TransducingPharmacologyAutophagyNeurodegenerationNeurodegenerative Diseasesmedicine.diseaseCell biologyHsp70Co-chaperone030104 developmental biologyProteasomeApoptosis Regulatory ProteinsTrends in pharmacological sciences
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Generation of three human iPSC lines from PLAN (PLA2G6-associated neurodegeneration) patients

2021

© 2021 The Authors.

0301 basic medicineQH301-705.5Cellular differentiationInduced Pluripotent Stem CellsNeuroaxonal Dystrophies:Cells::Stem Cells::Adult Stem Cells::Induced Pluripotent Stem Cells [ANATOMY]Biologymedicine.disease_cause:células::células madre::células madre adultas::células madre pluripotentes inducidas [ANATOMÍA]Sistema nerviós - DegeneracióCell LineDermal fibroblastGroup VI Phospholipases A203 medical and health sciencesKruppel-Like Factor 40302 clinical medicineSOX2medicineHumans:enfermedades del sistema nervioso::enfermedades neurodegenerativas [ENFERMEDADES]Biology (General)Induced pluripotent stem cellMutationNeurodegenerationCell DifferentiationCell BiologyGeneral Medicinemedicine.diseaseCellular Reprogramming030104 developmental biologyKLF4:Nervous System Diseases::Neurodegenerative Diseases [DISEASES]MutationCancer researchMalalties raresReprogramming030217 neurology & neurosurgeryGenèticaDevelopmental BiologyStem Cell Research
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