Search results for "DEGENERATION"

showing 10 items of 601 documents

β-Amyloid-induced activation of Caspase-3 in primary cultures of rat neurons

2000

It is known that beta-amyloid peptide (Abeta) contributes to the neurodegeneration in Alzheimer's disease (AD) and operates through activation of an apoptotic pathway. Apoptotic signal is driven by a family of cysteine proteases called caspases. The beta-amyloid precursor protein (APP) is directly and efficiently cleaved by caspases during apoptosis, resulting in elevated beta-amyloid peptide formation. Cerebellar neurons from rat pups were treated with the aged Abeta(25-35) at 1 and 5 microM and fluorescence assays of caspase activity performed over 4 days. We observed an increase in caspase activity after 48 h treatment in both 1 and 5 microM treated cells, then (72-96 h) caspase activity…

AgingTime FactorsAmyloidProteolysisApoptosisCaspase 3medicineAnimalsCells CulturedCaspaseNeuronsAmyloid beta-Peptidesbiologymedicine.diagnostic_testCaspase 3NeurodegenerationIntrinsic apoptosismedicine.diseaseMolecular biologyPeptide FragmentsRatsEnzyme Activationmedicine.anatomical_structureApoptosisCaspasesImmunologybiology.proteinNeuronDevelopmental BiologyMechanisms of Ageing and Development
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The emerging role of miRNA-132/212 cluster in neurologic and cardiovascular diseases: Neuroprotective role in cells with prolonged longevity

2021

Abstract miRNA-132/212 are small regulators of gene expression with a function that fulfills a vital function in diverse biological processes including neuroprotection of cells with prolonged longevity in neurons and the cardiovascular system. In neurons, miRNA-132 appears to be essential for controlling differentiation, development, and neural functioning. Indeed, it also universally promotes axon evolution, nervous migration, plasticity as well, it is suggested to be neuroprotective against neurodegenerative diseases. Moreover, miRNA-132/212 disorder leads to neural developmental perturbation, and the development of degenerative disorders covering Alzheimer’s, Parkinson’s, and epilepsy’s …

Agingmedicine.medical_specialtyNeurologyDegenerative Disordermedia_common.quotation_subjectNeuroprotection03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansMedicineMyocytes CardiacMolecular Targeted TherapyAxonCellular SenescenceComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonNeurons0303 health sciencesbusiness.industryNeurodegenerationAutophagyLongevityNeurodegenerative Diseasesmedicine.diseaseNeuroprotection3. Good healthMicroRNAsmedicine.anatomical_structureGene Expression RegulationCardiovascular DiseasesbusinessNeuroscience030217 neurology & neurosurgeryDevelopmental Biology
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Impaired calcium homeostasis in aged hippocampal neurons

2009

Abstract Development of neurodegenerative diseases such as Alzheimer's and Parkinson's disease is strongly age-associated. The impairment of calcium homeostasis is considered to be a key pathological event leading to neuronal dysfunction and cell death. However, the exact impact of aging on calcium homeostasis in neurons remains largely unknown. In the present work we have investigated intracellular calcium levels in cultured primary hippocampal neurons from young (2 months) and aged (24 months) rat brains. Upon stimulation with glutamate or hydrogen peroxide aged neurons in comparison to young neurons demonstrated an increased vulnerability to these disease-related toxins. Measurement of c…

Agingmedicine.medical_specialtyNeurotoxinsGlutamic Acidchemistry.chemical_elementHippocampusBiologyCalciumHippocampusCalcium in biologyRats Sprague-DawleyInternal medicinemedicineAnimalsCalcium SignalingOrganic ChemicalsCells CulturedCellular SenescenceNeuronsCalcium metabolismCalpainGeneral NeuroscienceNeurodegenerationGlutamate receptorCalpainHydrogen PeroxideOxidantsmedicine.diseaseRatsOxidative Stressmedicine.anatomical_structureEndocrinologynervous systemchemistryNerve Degenerationbiology.proteinCalciumNeuronNeuroscienceNeuroscience Letters
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Emerging contributions of formyl peptide receptors to neurodegenerative diseases.

2021

Abstract Inflammation is a central element of many neurodegenerative diseases. Formyl peptide receptors (FPRs) can trigger several receptor-dependent signal transduction pathways that play a key role in neuroinflammation and neurodegeneration. They are chemotactic receptors that help to regulate pro- and anti-inflammatory responses in most mammals. FPRs are primarily expressed in the immune and nervous systems where they interact with a complex pattern of pathogen-derived and host-endogenous molecules. Mounting evidence points towards a contribution of FPRs – via neuropathological ligands such as Amyloid beta, and neuroprotective ligands such as Humanin, Lipoxin A4, and Annexin A1 – to mult…

Amyloid beta-PeptidesClinical BiochemistryNeurodegenerationChemotaxisNeurodegenerative DiseasesBiologymedicine.diseaseLigandsBiochemistryNeuroprotectionReceptors Formyl PeptideNeuroinflammatory DiseasesmedicineFunctional selectivityAnimalsHumansSignal transductionMolecular BiologyCentral elementNeuroscienceNeuroinflammationHumaninBiological chemistryReferences
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Oxidative stress in Alzheimer’s Disease: Implications for Prevention and Therapy

2006

Oxidative stress is a marker of neurodegeneration and has been recently shown to be also involved in the early stages of the pathogenesis of various neurodegenerative disorders. In general, all biomolecules of the cell can be oxidized and thereby damaged. Consequently, the concept of neuroprotection by antioxidants has been developed. In many cases the direct scavanging of free radicals have been used as a strategy to prevent oxidative stress damage and a variety of physiological and synthetic antioxidant molecules have been identified and synthesized including the female sex homone estrogen. In Alzheimer’s Disease amyloid-β protein on its way to brain deposition can also induce oxidative c…

Amyloidbusiness.industryNeurodegenerationInflammationDNA oxidationBlood–brain barrierBioinformaticsmedicine.disease_causemedicine.diseaseProtein oxidationNeuroprotectionmedicine.anatomical_structuremedicinemedicine.symptombusinessOxidative stress
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The ALS-FTLD continuum: clinical, genetic and neuropsychological aspects

Amyotrophic lateral sclerosis frontotemporal lobar degeneration
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Successful subretinal delivery and monitoring of MicroBeads in mice

2013

BACKGROUND: To monitor viability of implanted genetically engineered and microencapsulated human stem cells (MicroBeads) in the mouse eye, and to study the impact of the beads and/or xenogenic cells on retinal integrity. METHODOLOGY/PRINCIPAL FINDINGS: MicroBeads were implanted into the subretinal space of SV126 wild type mice using an ab externo approach. Viability of microencapsulated cells was monitored by noninvasive retinal imaging (Spectralis™ HRA+OCT). Retinal integrity was also assessed with retinal imaging and upon the end of the study by light and electron microscopy. The implanted GFP-marked cells encapsulated in subretinal MicroBeads remained viable over a period of up to 4 mont…

Anatomy and PhysiologyMouseGreen Fluorescent Proteinslcsh:MedicineEyeRetinaMiceModel OrganismsMolecular Cell BiologyAnimalsHumansInherited Eye DisordersFluorescent Antibody Technique Indirectlcsh:ScienceBiologyMicroscopy ConfocalStem CellsRetinal Degenerationlcsh:RMesenchymal Stem CellsAnimal ModelsImmunohistochemistrySensory SystemsMicrospheresOphthalmoscopyOphthalmologyMicroscopy ElectronMedicineRetinal DisordersSurgerylcsh:QCellular TypesTomography Optical CoherenceResearch ArticleDevelopmental BiologyNeuroscienceStem Cell TransplantationPLoS ONE
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Collagens in the injured porcine intervertebral disc

1994

Spinal pain often is thought to be due to degeneration and mechanical failure of the intervertebral disc. Since the mechanical strength of the tissue depends on collagen fibers, the present study was designed to investigate the reactions in collagen metabolism after an experimentally induced disc injury. Five domestic pigs underwent an incision in the anterior part of the annulus fibrosus of disc L4-L5 through a retroperitoneal approach. The animals were killed 3 months postoperatively, and the injured discs and intact discs (controls) from different animals were removed for chemical analysis. Slices were cut from seven different parts across the disc. The concentration of total collagen (h…

Annulus (mycology)030222 orthopedicsPathologymedicine.medical_specialtyGranulation tissueIntervertebral discDegeneration (medical)Anatomy03 medical and health sciencesHydroxyprolinechemistry.chemical_compoundIntervertebral disk0302 clinical medicinemedicine.anatomical_structurechemistryCollagen metabolismmedicineOrthopedics and Sports MedicineNucleus030217 neurology & neurosurgeryJournal of Orthopaedic Research
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Novel imine antioxidants at low nanomolar concentrations protect dopaminergic cells from oxidative neurotoxicity.

2009

Strong evidence indicates that oxidative stress may be causally involved in the pathogenesis of Parkinson's disease. We have employed human dopaminergic neuroblastoma cells and rat primary mesencephalic neurons to assess the protective potential of three novel bisarylimine antioxidants on dopaminergic cell death induced by complex I inhibition or glutathione depletion. We have found that exceptionally low concentrations (EC(50) values approximately 20 nM) of these compounds (iminostilbene, phenothiazine, and phenoxazine) exhibited strong protective effects against the toxicities of MPP(+), rotenone, and l-buthionine sulfoximine. Investigating intracellular glutathione levels, it was found t…

Antioxidantmedicine.medical_treatmentDopamineGlutathione reductaseNeurotoxinsBiologymedicine.disease_causeProtein oxidationBiochemistryAntioxidantsLipid peroxidationRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumormedicineAnimalsHumansCells CulturedMembrane Potential MitochondrialCell DeathDose-Response Relationship DrugNeurotoxicityParkinson DiseaseRotenoneGlutathionemedicine.diseaseGlutathioneMitochondriaRatsSubstantia NigraOxidative StressNeuroprotective AgentschemistryBiochemistryElectron Transport Chain Complex ProteinsCytoprotectionNerve DegenerationIminesOxidation-ReductionOxidative stressJournal of neurochemistry
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Early structural degeneration of Mitroflow aortic valve: Another issue in addition to the mismatch?

2018

We reported two cases of early structural valve degeneration (SVD) with Mitroflow prosthesis in aortic position in patients above the age of 65 years. Microscopic aspects have been analysed to investigate the intrinsic mechanism of SVD. New techniques to improve the structure and the preservation of this prosthesis are needed in order to reduce potential dangerous early complications.

Aortic valvePulmonary and Respiratory Medicinemedicine.medical_specialtyAortic stenosimedicine.medical_treatmentCase ReportDegeneration (medical)030204 cardiovascular system & hematologyProsthesisStructural valve degeneration (SVD); aortic stenosis; prosthesis03 medical and health sciences0302 clinical medicineInternal medicinemedicineStructural valve degeneration (SVD)ProsthesiSettore MED/05 - Patologia ClinicaIn patient030212 general & internal medicineAortic stenosis; Prosthesis; Structural valve degeneration (SVD); Pulmonary and Respiratory Medicinebusiness.industryaortic stenosisSettore MED/23 - Chirurgia Cardiacamedicine.anatomical_structureCardiologyprosthesisbusiness
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