Search results for " STRESS"

showing 10 items of 3936 documents

Induction of Mitochondrial Changes Associated with Oxidative Stress on Very Long Chain Fatty Acids (C22:0, C24:0, or C26:0)-Treated Human Neuronal Ce…

2012

In Alzheimer's disease, lipid alterations point towards peroxisomal dysfunctions. Indeed, a cortical accumulation of saturated very long chain fatty acids (VLCFAs: C22:0, C24:0, C26:0), substrates for peroxisomalβ-oxidation, has been found in Alzheimer patients. This study was realized to investigate the effects of VLCFAs at the mitochondrial level since mitochondrial dysfunctions play crucial roles in neurodegeneration. On human neuronal SK-NB-E cells treated with C22:0, C24:0, or C26:0 (0.1–20 μM; 48 h), an inhibition of cell growth and mitochondrial dysfunctions were observed by cell counting with trypan blue, MTT assay, and measurement of mitochondrial transmembrane potential (Δψm) with…

AgingArticle SubjectMitochondrionBiologymedicine.disease_causeBiochemistryMitochondrial apoptosis-induced channelchemistry.chemical_compoundSuperoxidesCell Line TumormedicineHumanslcsh:QH573-671Cell ShapeCell ProliferationMembrane Potential MitochondrialNeuronslcsh:CytologySuperoxideFatty AcidsNeurodegenerationCell BiologyGeneral MedicinePeroxisomeFlow Cytometrymedicine.diseaseMolecular biologyMitochondriaCell biologyOxidative StressProtein SubunitsMicroscopy FluorescencechemistryMultiprotein ComplexesDNAJA3ATP–ADP translocaseOxidative stressResearch ArticleOxidative Medicine and Cellular Longevity
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Oxidative Stress and Mitochondrial Damage in Neurodegenerative Diseases: From Molecular Mechanisms to Targeted Therapies

2020

The progression of Alzheimer's dementia is associated with neurovasculature impairment, which includes inflammation, microthromboses, and reduced cerebral blood flow. Here, we investigate the effects of β amyloid peptides on the function of platelets, the cells driving haemostasis. Amyloid peptide β1-42 (Aβ1-42), Aβ1-40, and Aβ25-35 were tested in static adhesion experiments, and it was found that platelets preferentially adhere to Aβ1-42 compared to other Aβ peptides. In addition, significant platelet spreading was observed over Aβ1-42, while Aβ1-40, Aβ25-35, and the scAβ1-42 control did not seem to induce any platelet spreading, which suggested that only Aβ1-42 activates platelet signalli…

AgingArticle SubjectPlatelet Glycoprotein GPIIb-IIIa Complexmedicine.disease_causeBiochemistryOxidative Stress Mitochondria Neurodegenerative DiseasesText miningMedicineHumansPlatelet activationQH573-671business.industryNADPH OxidasesNeurodegenerative DiseasesThrombosisCell BiologyGeneral Medicinemedicine.diseasePlatelet ActivationThrombosisPlatelet Glycoprotein GPIIb-IIIa ComplexOxidative StressCancer researchCytologybusinessOxidative stressResearch ArticleOxidative Medicine and Cellular Longevity
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Pro-inflammatory genetic background and zinc status in old atherosclerotic subjects.

2008

Inflammation and genetics are prominent mechanisms in the pathogenesis of atherosclerosis (AT) and its complications. In this review we discuss the possible impact on AT development of several genetic determinants involved in inflammation, oxidative stress and cytoprotection (IL-6, TNF-alpha, IL-10, CD14, TLR4, MT, HSP70). Genetic polymorphisms of these genes may affect a differential inflammatory response predisposing to AT. However, allelic polymorphisms of genes which increase the risk of AT frequently occur in the general population but, only adequate gene-environment-polymorphism interactions promote the onset of the disease. Zinc deficiency has been suggested as an environmental risk …

AgingCandidate genePopulationInflammationDiseaseBiologymedicine.disease_causeBiochemistryPathogenesisAgeing atherosclerosis inflammation geneticsmedicineSettore MED/05 - Patologia ClinicaHomeostasisHumansAlleleeducationMolecular BiologyAgedSettore MED/04 - Patologia GeneraleAged 80 and overInflammationeducation.field_of_studymedicine.diseaseAtherosclerosisOxidative StressZincNeurologyImmunologyZinc deficiencyMetallothioneinmedicine.symptomOxidative stressBiotechnologyAgeing research reviews
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Oxidative stress and xenobiotic detoxification enzymes in rat astrocytes: Correlations with brain aging

2012

Meeting Abstract; International audience

AgingChemistry[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontology[ SDV.TOX ] Life Sciences [q-bio]/ToxicologyCell Biology[ SDV.MHEP.GEG ] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyDetoxification enzymesmedicine.disease_causeBiochemistrychemistry.chemical_compoundEndocrinologyBiochemistry[SDV.TOX]Life Sciences [q-bio]/ToxicologyGeneticsmedicineXenobioticMolecular BiologyBrain agingOxidative stressComputingMilieux_MISCELLANEOUS
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Resilience and Psychobiological Response to Stress in Older People: The Mediating Role of Coping Strategies

2021

Resilience, the ability to overcome adversity and face stressful demands and experiences, has been strongly associated with successful aging, a low risk of diseases and high mental and physical functioning. This relationship could be based on adaptive coping behaviors, but more research is needed to gain knowledge about the strategies employed to confront social stress. Thus, we aimed to investigate the role of the use of active or passive coping strategies by resilient people in dealing with stressful situations. For this purpose, we measured resilience, coping strategies, and perceived stress in 66 healthy older adults (31 men and 35 women) between 56 and 75 years old who were exposed to …

AgingCoping (psychology)Cognitive Neurosciencemedia_common.quotation_subject030209 endocrinology & metabolismcortisollcsh:RC321-571older people03 medical and health sciencesstress0302 clinical medicinemedicineTrier social stress testresiliencelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal Researchmedia_commonSocial stressSuccessful agingStressorcopingAnxietyPsychological resiliencemedicine.symptomPsychologyPsychosocial030217 neurology & neurosurgeryNeuroscienceClinical psychologyFrontiers in Aging Neuroscience
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Acute psychosocial stress effects on memory performance: Relevance of age and sex.

2018

In recent decades, there has been a growing interest in investigating the effects of chronic and acute stress on cognitive processes, especially memory performance. However, research focusing on acute stress effects has reported contradictory findings, probably due to the many factors that can moderate this relationship. In addition to factors related to the individual, such as sex and age, other factors, such as the type of memory assessed, can play a critical role in the direction of these effects. This review summarizes the main findings of our research group and others about the effects of acute psychosocial stress on memory performance in young and older people of both sexes, taking in…

AgingEMOTIONAL MEMORYCognitive NeuroscienceExperimental and Cognitive PsychologySALIVARY ALPHA-AMYLASENeuropsychological TestsMemory performancePsychosocial stressCortisol050105 experimental psychologyDevelopmental psychology03 medical and health sciencesBehavioral NeuroscienceWORKING-MEMORY0302 clinical medicineSex FactorsMemoryMedicine and Health SciencesRelevance (law)Humans0501 psychology and cognitive sciencesSOCIAL STRESSSocial stressWorking memoryLong-term memory05 social sciencesStressorAge FactorsCognitionNORADRENERGIC ACTIVATIONNON-DECLARATIVE MEMORYLONG-TERM-MEMORYMemory Short-TermHPA AXISCORTISOL-LEVELSPsychosocial stressMental RecallSexPRE-LEARNING STRESSINDUCEDPsychologyNeuroscience030217 neurology & neurosurgeryStress PsychologicalNeurobiology of learning and memory
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Mitochondrial oxidative stress plays a key role in aging and apoptosis

2000

Harman first suggested in 1972 that mitochondria might be the biological clock in aging, noting that the rate of oxygen consumption should determine the rate of accumulation of mitochondrial damage produced by free radical reactions. Later in 1980 Miquel and coworkers proposed the mitochondrial theory of cell aging. Mitochondria from postmitotic cells use O2 at a high rate, hence releasing oxygen radicals that exceed the cellular antioxidant defences. The key role of mitochondria in cell aging has been outlined by the degeneration induced in cells microinjected with mitochondria isolated from fibroblasts of old rats, especially by the inverse relationship reported between the rate of mitoch…

AgingFree RadicalsClinical BiochemistryApoptosisOxidative phosphorylationMitochondrionBiologymedicine.disease_causeDNA MitochondrialBiochemistryLipid peroxidationMicechemistry.chemical_compoundGeneticsmedicineCardiolipinAnimalsHumansMolecular BiologyFree-radical theory of agingchemistry.chemical_classificationReactive oxygen speciesBrainCell BiologyGlutathioneMitochondriaOxygenOxidative StressLiverchemistryBiochemistryCell agingOxidative stress
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Up-Regulation of leucocytes Genes Implicated in Telomere Dysfunction and Cellular Senescence Correlates with Depression and Anxiety Severity Scores

2012

BACKGROUND: Major depressive disorder (MDD) is frequently associated with chronic medical illness responsible of increased disability and mortality. Inflammation and oxidative stress are considered to be the major mediators of the allostatic load, and has been shown to correlate with telomere erosion in the leucocytes of MDD patients, leading to the model of accelerated aging. However, the significance of telomere length as an exclusive biomarker of aging has been questioned on both methodological and biological grounds. Furthermore, telomeres significantly shorten only in patients with long lasting MDD. Sensitive and dynamic functional biomarkers of aging would be clinically useful to eval…

AgingGene Expressionlcsh:MedicineAnxietySocial and Behavioral Sciences0302 clinical medicineBiomarkers of agingMolecular Cell BiologyLeukocytesPathologyPsychologylcsh:ScienceCellular SenescenceDepression (differential diagnoses)Psychiatry0303 health sciencesMultidisciplinaryDepressionChromosome BiologyGenomicsMiddle AgedTelomereAllostatic loadUp-RegulationTelomeresMental HealthMedicineMajor depressive disorderAnxietyBiomarker (medicine)Femalemedicine.symptomResearch ArticleAdultSenescenceClinical PathologyPsychological StressBiologybehavioral disciplines and activitiesMolecular Genetics03 medical and health sciencesDiagnostic Medicinemental disordersGeneticsmedicineHumansBiologyCyclin-Dependent Kinase Inhibitor p16030304 developmental biologyDepressive Disorder Majorlcsh:RComputational BiologyHuman GeneticsDNAmedicine.diseaseTelomereOxygenGene Expression RegulationImmunologyStathminlcsh:QBiomarkers030217 neurology & neurosurgeryDNA DamagePLoS ONE
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Brain aging and late-onset Alzheimer's disease: many open questions.

2012

ABSTRACTDespite decades of research in the field of Alzheimer's disease (AD), a real understanding of its molecular pathophysiology and treatments relevant to the day-to-day lives of patients remain out of reach. Research has, with good reason, focused on certain key pathways and potential mechanisms, but sometimes this has been at the expense of work on other theories, which may be slowing down progress in this field. Interesting theories at present include oxidative stress and caloric restriction. Work on the Aβ cascade should continue but with a shift in focus to its intracellular effects and an awareness that additional pathogenetic factors and processes must be involved – most importan…

AgingHyperphosphorylationLate onsettau ProteinsDiseaseEpigenesis GeneticAmyloid beta-Protein PrecursorAlzheimer DiseaseIntervention (counseling)MedicineDementiaAnimalsHumansEpigeneticsCaloric Restrictionbusiness.industryNeurodegenerationBrainmedicine.diseasePsychiatry and Mental healthClinical PsychologyOxidative StressGeriatrics and GerontologyAlzheimer's diseasebusinessGerontologyNeuroscienceInternational psychogeriatrics
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Inflammation and oxidative stress in vertebrate host–parasite systems

2008

Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms. Inflammation relies on a number of cellular and molecular effectors that can strike invading pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-specific way. Owing to this non-specific response, inflammation can generate substantial costs for the host if the inflammatory response, and the associated oxygen-based damage, get out of control. This imposes strong selection pressure that acts to optimize two key features of the inflammatory response: the timing of activation and resolution (the process of downregulation of the response). In this p…

AgingInflammationReviewBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyHost-Parasite InteractionsImmune systemDownregulation and upregulationImmunitymedicineAnimalsHomeostasisHumansSelection GeneticInflammationInnate immune systemEffectorReactive Nitrogen SpeciesImmunity InnateOxidative StressImmunologymedicine.symptomReactive Oxygen SpeciesGeneral Agricultural and Biological SciencesHomeostasisOxidative stressPhilosophical Transactions of the Royal Society B: Biological Sciences
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