Search results for "Amy"

showing 10 items of 1486 documents

Antioxidant Pathways in Alzheimers Disease: Possibilities of Intervention

2011

Alzheimer's disease (AD) is closely related to the occurrence of oxidative stress. It was claimed that all pathophysiological mechanisms involved in the onset and progression of AD are related to oxidative stress. Thus, it is important to evaluate if there is oxidative stress as well as the mechanism by which this happens in AD patients as well as in animal models of AD. Extracellular plaques of amyloid b peptides (Aβ), a hallmark of the disease, have been postulated to be more protective than damaging in terms of oxidative stress because they may be chemical sinks in which heavy metals are placed. More than a decade ago we reasoned that damage due to Ab might be caused not by extracellular…

AntioxidantAmyloidmedicine.medical_treatmentRespiratory chainNerve Tissue ProteinsBiologyPharmacologymedicine.disease_causeAntioxidantsAlzheimer DiseaseDrug DiscoverymedicineExtracellularAnimalsHumansMolecular Targeted TherapyPharmacologychemistry.chemical_classificationReactive oxygen speciesEstradiolVitamin Emedicine.diseaseUp-RegulationOxidative StressNeuroprotective AgentschemistryDietary SupplementsImmunologyAlzheimer's diseaseReactive Oxygen SpeciesOxidative stressCurrent Pharmaceutical Design
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Antioxidant and glutathione-related enzymatic activities in rat sciatic nerve

1990

Abstract The present work tries to establish the antioxidant capacity of the peripheral nervous tissue of the rat, in terms of the enzymatic activities present in this tissue that either prevent the formation of activated species as the semiquinone radical (DT-diaphorase), protect against activated oxygen species (superoxide dismutase, glutathione peroxidase), conjugate natural toxic products or xenobiotics (glutathione S-transferases, especially the activity conjugating 4-hydroxy-nonenal), or complete the glutathione system metabolism (glutathione disulfide reductase, γ-glutamyl transpeptidase). All the activities studied are lower in this tissue than they are in liver, except for γ-glutam…

AntioxidantGPX3medicine.medical_treatmentGlutathione reductaseToxicologyAntioxidantsSuperoxide dismutaseCellular and Molecular Neurosciencechemistry.chemical_compoundDevelopmental NeurosciencemedicineAnimalsQuinone ReductasesGlutathione Transferasechemistry.chemical_classificationGlutathione PeroxidasebiologySuperoxide DismutaseChemistryGlutathione peroxidaseNervous tissuegamma-GlutamyltransferaseGlutathioneGlutathioneSciatic NerveRatsGlutathione S-transferasemedicine.anatomical_structureBiochemistrybiology.proteinNeurotoxicology and Teratology
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The role of glutathione in protection against DNA damage induced by rifamycin SV and copper(II) ions.

1993

Incubation of calf thymus DNA in the presence of rifamycin SV induces a decrease in the absorbance of DNA at 260 nm. The effect, was found to be proportional to the antibiotic concentration and enhanced by copper(II) ions. In the presence of rifamycin SV and copper(II), a significant increase in thiobarbituric acid-reactive (TBA-reactive) material is also observed. This effect is inhibited to different degrees by the following antioxidants: catalase 77%; thiourea 72%; glutathione (GSH) 62%; ethanol 52%; and DMSO 34%, suggesting that both hydrogen peroxide (H2O2) and hydroxyl radicals (OH.) are involved in DNA damage. Rifamycin SV-copper(II) mixtures were also found to induce the production …

AntioxidantbiologyEthanolChemistryDNA damagemedicine.medical_treatmentRadicalThioureaRifamycinGlutathioneDNABiochemistryGlutathioneRifamycinsThiobarbituric Acid Reactive Substanceschemistry.chemical_compoundOxygen ConsumptionDeoxyriboseBiochemistryCatalasebiology.proteinmedicineHydrogen peroxideCopperDNA DamageFree radical research communications
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Amyloid-β toxicity and tau hyperphosphorylation are linked via RCAN1 in Alzheimer's disease.

2011

Amyloid-β peptide (Aβ) toxicity and tau hyperphosphorylation are hallmarks of Alzheimer’s disease (AD). How their molecular relationships may affect the etiology, progression, and severity of the disease, however, has not been elucidated. We now report that incubation of foetal rat cortical neurons with Aβ up-regulates expression of the Regulator of Calcineurin gene RCAN1, and this is mediated by Aβ-induced oxidative stress. Calcineurin (PPP3CA) is a serine-threonine phosphatase that dephosphorylates tau. RCAN1 proteins inhibit this phosphatase activity of calcineurin. Increased expression of RCAN1 also causes up-regulation of glycogen synthase kinase-3beta (GSK3β), a tau kinase. Thus, incr…

Apolipoprotein EAdultMuscle Proteinstau ProteinsBiologymedicine.disease_causeTransfectionArticleDephosphorylationGlycogen Synthase Kinase 3GSK-3Alzheimer DiseasemedicineAnimalsHumansLymphocytesPhosphorylationRNA Small InterferingGSK3BCells CulturedChromatography High Pressure LiquidRegulation of gene expressionCerebral CortexNeuronsAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaGeneral NeuroscienceCalcineurinIntracellular Signaling Peptides and ProteinsGeneral MedicineMiddle Agedmedicine.diseaseEmbryo MammalianMolecular biologyGlutathionePeptide FragmentsCell biologyRatsCalcineurinDNA-Binding ProteinsPsychiatry and Mental healthClinical PsychologyOxidative StressGene Expression RegulationFemaleGeriatrics and GerontologyAlzheimer's diseaseOxidative stressJournal of Alzheimer's disease : JAD
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Functional Role of Lipoprotein Receptors in Alzheimers Disease

2008

The LDL receptor gene family constitutes a class of structurally closely related cell surface receptors fulfilling diverse functions in different organs, tissues, and cell types. The LDL receptor is the prototype of this family, which also includes the VLDLR, ApoER2/LRP8, LRP1 and LRP1B, as well as Megalin/GP330, SorLA/LR11, LRP5, LRP6 and MEGF7. Recently several lines of evidence have positioned the LDL receptor gene family as one of the key players in Alzheimer's disease (AD) research. Initially this receptor family was of high interest due to its key function in cholesterol/apolipoprotein E (ApoE) uptake, with the epsilon4 allele of ApoE as the strongest genetic risk factor for late-onse…

Apolipoprotein EAmyloid beta-PeptidesbiologyChemistryEndosomeLRP1BLRP1Cell biologyAmyloid beta-Protein PrecursorApolipoproteins ECholesterolReceptors LDLNeurologyAlzheimer DiseaseCell surface receptormental disordersLDL receptorAmyloid precursor proteinbiology.proteinAnimalsHumansNeurology (clinical)ReceptorCurrent Alzheimer Research
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Apolipoprotein E Regulates Amyloid Formation within Endosomes of Pigment Cells.

2015

International audience; Accumulation of toxic amyloid oligomers is a key feature in the pathogenesis of amyloid-related diseases. Formation of mature amyloid fibrils is one defense mechanism to neutralize toxic prefibrillar oligomers. This mechanism is notably influenced by apolipoprotein E variants. Cells that produce mature amyloid fibrils to serve physiological functions must exploit specific mechanisms to avoid potential accumulation of toxic species. Pigment cells have tuned their endosomes to maximize the formation of functional amyloid from the protein PMEL. Here, we show that ApoE is associated with intraluminal vesicles (ILV) within endosomes and remain associated with ILVs when th…

Apolipoprotein EAmyloidAmyloidEndosome[SDV.BC]Life Sciences [q-bio]/Cellular BiologyEndosomesBiologyExosomesGeneral Biochemistry Genetics and Molecular BiologyMiceApolipoproteins Emental disordersAnimalsHumansamyloid-related diseaseslcsh:QH301-705.5[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMelanosomeMice KnockoutMelanosomesEndosomal Sorting Complexes Required for TransportVesicleMicrovesiclesPMELCell biologyMice Inbred C57BLlcsh:Biology (General)BiochemistryGene Expression RegulationMelanocytesSignal transductionHeLa CellsSignal TransductionCell reports
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Functional role of the low-density lipoprotein receptor-related protein in Alzheimer's disease.

2006

Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder, characterized by neuronal loss, neurofibrillary tangle formation and the extracellular deposition of amyloid-β (Aβ) plaques. The amyloid precursor protein (APP) and the enzymes responsible for Aβ generation seem to be the base elements triggering the destructive processes. Initially, the low-density lipoprotein receptor-related protein (LRP) was genetically linked to AD and later it emerged to impact on many fundamental events related to this disease. LRP is not only involved in Aβ clearance but is also the major receptor of several AD-associated ligands, e.g. apolipoprotein E and α<sub>2</sub>-m…

Apolipoprotein EFunctional rolemedicine.medical_specialtyPathologybiologyChemistryDiseaseLRP1Amyloid beta-Protein PrecursorEndocrinologyNeurologyAlzheimer DiseaseInternal medicineLDL receptormedicineExtracellularAmyloid precursor proteinbiology.proteinNeurofibrillary tangle formationAnimalsHumansNeurology (clinical)LDL-Receptor Related ProteinsNeuro-degenerative diseases
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Haptoglobin interacts with apolipoprotein E and beta-amyloid and influences their crosstalk.

2014

Beta-amyloid accumulation in brain is a driving force for Alzheimer's disease pathogenesis. Apolipoprotein E (ApoE) represents a critical player in beta-amyloid homeostasis, but its role in disease progression is controversial. We previously reported that the acute-phase protein haptoglobin binds ApoE and impairs its function in cholesterol homeostasis. The major aims of this study were to characterize the binding of haptoglobin to beta-amyloid, and to evaluate whether haptoglobin affects ApoE binding to beta-amyloid. Haptoglobin is here reported to form a complex with beta-amyloid as shown by immunoblotting experiments with purified proteins, or by its immunoprecipitation in brain tissues …

Apolipoprotein EMalePhysiologyDiseaseBeta-amyloidBiochemistryAmyloid beta-Protein PrecursorAlzheimer' diseasepolycyclic compoundsskin and connective tissue diseasesapolipoprotein EbiologyChemistryMedicine (all)Haptoglobinfood and beveragesBrainApoE/A? complexGeneral MedicineMiddle AgedhaptoglobinCrosstalk (biology)ApoE/Aβ complexSettore MED/26 - Neurologialipids (amino acids peptides and proteins)FemaleAlzheimer's diseaseProtein BindingAdultmedicine.medical_specialtyImmunoprecipitationCognitive NeuroscienceEnzyme-Linked Immunosorbent AssayCHO CellsTransfectionAlzheimer' disease; ApoE/Aβ complex; Apolipoprotein E; Beta-amyloid; Haptoglobin; Human brain tissue; Adult; Aged; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Analysis of Variance; Animals; Apolipoproteins E; Brain; CHO Cells; Cricetulus; Enzyme-Linked Immunosorbent Assay; Female; Haptoglobins; Humans; Immunoprecipitation; Male; Middle Aged; Mutation; Protein Binding; Transfection; Biochemistry; Cell Biology; Physiology; Cognitive Neuroscience; Medicine (all)NOApolipoproteins ECricetulusAlzheimer DiseaseInternal medicinemental disordersmedicineAnimalsHumansImmunoprecipitationAgedAnalysis of VarianceAmyloid beta-PeptidesHaptoglobinsNeurotoxicityAlzheimer’diseaseCell Biologymedicine.diseasehuman brain tissueEndocrinologyMutationbiology.proteinAlzheimer'diseaseHomeostasisACS chemical neuroscience
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Apolipoprotein E polymorphism influences not only cerebral senile plaque load but also Alzheimer-type neurofibrillary tangle formation.

1995

Only recently, evidence was provided that apolipoprotein E allele epsilon 4 located on Chromosome 19 is associated with late onset (i.e. senile) sporadic Alzheimer's disease. Histologically, Alzheimer's disease is associated with intraneuronal neurofibrillary changes and extraneuronal A4/beta-amyloid deposition. We set out with a histological staging system which considers the gradual development of Alzheimer's disease-related histological changes over time and correlates highly with the cognitive decline ante mortem. Our analysis revealed that both the mean stage for A4/beta-amyloid deposits and the mean stage for neurofibrillary tangles get significantly shifted upwards in epsilon 4-carri…

Apolipoprotein EPathologymedicine.medical_specialtyGenotypeLate onsetBiologyCentral nervous system diseaseDegenerative diseaseApolipoproteins EAlzheimer DiseasemedicineHumansSenile plaquesCognitive declineAllelesAgedAged 80 and overAmyloid beta-PeptidesPolymorphism GeneticGeneral NeuroscienceAge FactorsBrainNeurofibrillary tangleNeurofibrillary TanglesMiddle Agedmedicine.diseaseRegression AnalysisAlzheimer's diseaseChromosomes Human Pair 19Neuroscience
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Energetic coupling between plastids and mitochondria drives CO2 assimilation in diatoms.

2015

International audience; Diatoms are one of the most ecologically successful classes of photosynthetic marine eukaryotes in the contemporary oceans. Over the past 30 million years, they have helped to moderate Earth's climate by absorbing carbon dioxide from the atmosphere, sequestering it via the biological carbon pump and ultimately burying organic carbon in the lithosphere. The proportion of planetary primary production by diatoms in the modern oceans is roughly equivalent to that of terrestrial rainforests. In photosynthesis, the efficient conversion of carbon dioxide into organic matter requires a tight control of the ATP/NADPH ratio which, in other photosynthetic organisms, relies prin…

Aquatic Organismschemistry.chemical_compoundAdenosine TriphosphateSettore BIO/04 - Fisiologia VegetaleCYCLIC ELECTRON FLOWPlastidsPhotosynthesisPHAEODACTYLUM-TRICORNUTUMPlant Proteinschemistry.chemical_classificationMultidisciplinarymicroalgaeRespirationCarbon fixationEnergetic interactionsProton-Motive ForceMitochondriametabolic mutantPhenotypeATP/NADPH ratioOXYGEN PHOTOREDUCTIONCarbon dioxideOxidoreductasesOxidation-ReductionOceanOceans and SeasElectron flowMarine eukaryotesBiologyPhotosynthesisCHLAMYDOMONAS-REINHARDTIICarbon cycleCarbon CycleMitochondrial ProteinsEnergetic exchangesBotanyOrganic matterEcosystem[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology14. Life underwaterPlastidEcosystemDiatomsChemiosmosisfungiECSCarbon Dioxidechemistry13. Climate actionNADP
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