Search results for "YLOID"

showing 10 items of 526 documents

Life history adjustments to intestinal inflammation in a gut nematode.

2017

ABSTRACT Many parasitic nematodes establish chronic infections. This implies a finely tuned interaction with the host immune response in order to avoid infection clearance. Although a number of immune interference mechanisms have been described in nematodes, how parasites adapt to the immune environment provided by their hosts remains largely unexplored. Here, we used the gastrointestinal nematode Heligmosomoides polygyrus to investigate the plasticity of life history traits and immunomodulatory mechanisms in response to intestinal inflammation. We adopted an experimental model of induced colitis and exposed worms to intestinal inflammation at two different developmental stages (larvae and …

0301 basic medicinePhysiologyPhenotypic plasticityAquatic ScienceHost-Parasite InteractionsImmunomodulation03 medical and health sciencesMice0302 clinical medicineImmune systemparasitic diseases[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosismedicine[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyAnimalsColitisAdaptationIntestinal Diseases ParasiticMolecular BiologyLife History TraitsEcology Evolution Behavior and SystematicsStrongylida InfectionsInfectivityInflammationStrongyloideaPhenotypic plasticityMice Inbred BALB CbiologyHost (biology)Dextran SulfateInflammatory responseHelminth Proteinsmedicine.diseasebiology.organism_classification3. Good healthIntestinesDisease Models Animal030104 developmental biologyNematodeInfectivityInsect ScienceLarvaImmunology[SDV.IMM]Life Sciences [q-bio]/ImmunologyAnimal Science and ZoologyHeligmosomoides polygyrusAdaptation030215 immunology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/SymbiosisThe Journal of experimental biology
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PTEN recruitment controls synaptic and cognitive function in Alzheimer's models

2016

Dyshomeostasis of amyloid-β peptide (Aβ) is responsible for synaptic malfunctions leading to cognitive deficits ranging from mild impairment to full-blown dementia in Alzheimer's disease. Aβ appears to skew synaptic plasticity events toward depression. We found that inhibition of PTEN, a lipid phosphatase that is essential to long-term depression, rescued normal synaptic function and cognition in cellular and animal models of Alzheimer's disease. Conversely, transgenic mice that overexpressed PTEN displayed synaptic depression that mimicked and occluded Aβ-induced depression. Mechanistically, Aβ triggers a PDZ-dependent recruitment of PTEN into the postsynaptic compartment. Using a PTEN kno…

0301 basic medicinePrimary Cell CulturePDZ DomainsMice TransgenicMolecular neuroscienceBiologyNeurotransmissionSynaptic TransmissionMice03 medical and health sciences0302 clinical medicineAlzheimer DiseasePostsynaptic potentialmedicineAnimalsPTENGene Knock-In TechniquesAmyloid beta-PeptidesGeneral NeurosciencePTEN PhosphohydrolaseLong-term potentiationmedicine.diseaseRatsDisease Models Animal030104 developmental biologySynaptic fatigueSynaptic plasticitybiology.proteinAlzheimer's diseaseCognition DisordersNeuroscience030217 neurology & neurosurgeryNature Neuroscience
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Aβ Induces Excitotoxicity Mediated by APC/C-Cdh1 Depletion That Can Be Prevented by Glutaminase Inhibition Promoting Neuronal Survival

2016

AbstractThe E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) is activated by the fizzy-related protein homolog/CDC20-like protein 1 (cdh1) in post-mitotic neurons. Growing evidence suggests that dysregulation of APC/C-Cdh1 is involved in neurodegenerative diseases. Here we show in neurons that oligomers of amyloid beta (Aβ), a peptide related to Alzheimer’s disease, cause proteasome-dependent degradation of cdh1. This leads to a subsequent increase in glutaminase (a degradation target of APC/C-Cdh1), which causes an elevation of glutamate levels and further intraneuronal Ca2+ dysregulation, resulting in neuronal apoptosis. Glutaminase inhibition prevents glutamate excitotoxi…

0301 basic medicineProteasome Endopeptidase ComplexCell SurvivalAmyloid betaBlotting WesternExcitotoxicityHippocampusmedicine.disease_causeHippocampusArticleAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsAnimals Genetically ModifiedMice03 medical and health sciences0302 clinical medicineGlutaminasemedicineAnimalsRats WistarNeuronsAmyloid beta-PeptidesMultidisciplinarybiologyGlutaminaseCyclin-dependent kinase 5Glutamate receptorCyclin-Dependent Kinase 5Molecular biologyRatsUbiquitin ligase030104 developmental biologyApoptosisbiology.protein030217 neurology & neurosurgeryScientific Reports
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Phosphorylation of meprin β controls its cell surface abundance and subsequently diminishes ectodomain shedding

2021

Meprin β is a zinc-dependent metalloprotease exhibiting a unique cleavage specificity with strong preference for acidic amino acids at the cleavage site. Proteomic studies revealed a diverse substrate pool of meprin β including the interleukin-6 receptor (IL-6R) and the amyloid precursor protein (APP). Dysregulation of meprin β is often associated with pathological conditions such as chronic inflammation, fibrosis, or Alzheimer's disease (AD). The extracellular regulation of meprin β including interactors, sheddases, and activators has been intensively investigated while intracellular regulation has been barely addressed in the literature. This study aimed to analyze C-terminal phosphorylat…

0301 basic medicineProtein Kinase C-alphaImmunoprecipitationmedia_common.quotation_subjectBiochemistry03 medical and health sciences0302 clinical medicineProtein Kinase C betaTumor Cells CulturedGeneticsAmyloid precursor proteinHumansPhosphorylationInternalizationMolecular BiologyProtein kinase Cmedia_commonbiologyChemistryCell MembraneMetalloendopeptidasesSheddaseCell biology030104 developmental biologyGene Expression RegulationEctodomainColonic NeoplasmsProteolysisbiology.proteinPhosphorylationExtracellular Space030217 neurology & neurosurgeryIntracellularBiotechnologyThe FASEB Journal
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Association between urticaria and nematode infections

2018

Background The association between parasites and urticaria was first suggested in the last century. A wide range, 0-75.4%, of the prevalence of parasitic infection has been reported with chronic urticaria (CU). Moreover, urticaria may be detected in patients with parasitosis. Nematodes are a type of helminth that infect hundreds of millions of people throughout the world. Objective The aim of this work was to collect and review the published studies and cases of urticaria associated with nematode infections. Methods A search of scientific literature data bases from January 1960 until May 2017 was carried out. Results Numerous nematode infections have been associated with urticaria and/or an…

0301 basic medicinePulmonary and Respiratory Medicine030103 biophysicsmedicine.medical_specialtyUrticariamedicine.disease_causeNecator americanusStrongyloides stercoralisallergic immunoglobulin03 medical and health sciencesSpecies Specificityimmune system diseasesparasitic diseasesAscaridoideaHelminthMedicineAnimalsHumansImmunology and AllergyAngioedemaAntigensskin and connective tissue diseasesDirofilariaSkinGnathostomaMansonella streptocercabiologyAngioedemabusiness.industryGeneral MedicineAllergensImmunoglobulin Ebiology.organism_classificationDermatologyAscaridida InfectionsWuchereria bancroftiItalyAntigens HelminthAllergens; Angioedema; Animals; Antigens Helminth; Ascaridida Infections; Ascaridoidea; Humans; Immunoglobulin E; Italy; Skin; Species Specificity; Urticariamedicine.symptomLoa loabusiness
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Regulatory effects of simvastatin and apoJ on APP processing and amyloid-beta clearance in blood-brain barrier endothelial cells

2017

Amyloid-β peptides (Aβ) accumulate in cerebral capillaries indicating a central role of the blood-brain barrier (BBB) in the pathogenesis of Alzheimer’s disease (AD). Although a relationship between apolipoprotein-, cholesterol- and Aβ metabolism is evident, the interconnecting mechanisms operating in brain capillary endothelial cells (BCEC) are poorly understood. ApoJ (clusterin) is present in HDL that regulates cholesterol metabolism which is disturbed in AD. ApoJ levels are increased in AD brains and in plasma of cerebral amyloid angiopathy (CAA) patients. ApoJ may bind, prevent fibrillization, and enhance clearance of Aβ. We here define a connection of apoJ and cellular cholesterol home…

0301 basic medicineSimvastatinmedicine.medical_specialtyAmyloidSwineMice TransgenicBiologyBlood–brain barrierAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineInternal medicinemedicineAmyloid precursor proteinAnimalsMolecular BiologyCells CulturedAmyloid beta-PeptidesClusterinEndothelial CellsCell Biologymedicine.diseaseLRP1Peptide FragmentsMice Inbred C57BLClusterin030104 developmental biologyEndocrinologymedicine.anatomical_structureBlood-Brain Barrierbiology.proteinFemaleCerebral amyloid angiopathyblood-brain barrier ; amyloid-β ; cholesterol ; simvastatin ; clusterin/apoJ ; LRP1Protein Processing Post-Translational030217 neurology & neurosurgeryIntracellularLipoprotein
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Pressure effects on α-synuclein amyloid fibrils: An experimental investigation on their dissociation and reversible nature

2017

α–synuclein amyloid fibrils are found in surviving neurons of Parkinson's disease affected patients, but the role they play in the disease development is still under debate. A growing number of evidences points to soluble oligomers as the major cytotoxic species, while insoluble fibrillar aggregates could even play a protection role. In this work, we investigate α–synuclein fibrils dissociation induced at high pressure by means of Small Angle X-ray Scattering and Fourier Transform Infrared Spectroscopy. Fibrils were produced from wild type α–synuclein and two familial mutants, A30P and A53T. Our results enlighten the different reversible nature of α–synuclein fibrils fragmentati…

0301 basic medicineSmall AngleAmyloidHigh-pressureMutantBiophysicsmacromolecular substances010402 general chemistryFibril01 natural sciencesBiochemistryDissociation (chemistry)Scattering03 medical and health scienceschemistry.chemical_compoundX-Ray DiffractionScattering Small AngleSpectroscopy Fourier Transform InfraredPressureHumansPoint MutationFourier transform infrared spectroscopyMolecular BiologySpectroscopyAlpha-synucleinAmyloid; FTIR; High-pressure; SAXS; α-synuclein; Amyloid; Humans; Parkinson Disease; Point Mutation; Pressure; Scattering Small Angle; Solubility; Spectroscopy Fourier Transform Infrared; X-Ray Diffraction; alpha-Synuclein; Biophysics; Biochemistry; Molecular BiologySmall-angle X-ray scatteringWild typeα-synucleinParkinson DiseaseSAXSAmyloid fibril0104 chemical sciences?-synucleinCrystallography030104 developmental biologyBiophysicchemistryFTIRSolubilityFourier Transform InfraredBiophysicsalpha-SynucleinHuman
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A Shotgun Proteomics Approach Reveals a New Toxic Role for Alzheimer's Disease Aβ Peptide: Spliceosome Impairment.

2017

Proteomic changes have been described in many neurodegenerative diseases, including Alzheimer's disease (AD). However, the early events in the onset of the pathology are yet to be fully elucidated. A cell model system in which LAN5 neuroblastoma cells were incubated for a short time with a recombinant form of Aβ42 was utilized. Proteins extracted from these cells were subjected to shotgun proteomics analysis by LTQ-Orbitrap-MS followed by label-free quantitation. By bioinformatics tools we found that the most significant of those found to be up-regulated were related to cytoskeletal dynamics (Rho related) and membrane-related processes. The most significant of the down-regulated proteins we…

0301 basic medicineSpliceosomeAmyloid beta-PeptideProteomeComputational biologyDiseaseBiologyBiochemistrylaw.inventionearly events in AD03 medical and health sciencesNeuroblastoma0302 clinical medicinelawAlzheimer DiseaseCell Line TumorHumansShotgun proteomicsCytoskeletonCytoskeletonGeneticsAmyloid beta-PeptidesChemistry (all)Cell MembraneGeneral ChemistryRibosomal RNAAlzheimer's diseaseRecombinant Proteinshotgun proteomicRecombinant Proteins030104 developmental biologySpliceosomeGene Expression RegulationRNA splicingRecombinant DNASpliceosomes030217 neurology & neurosurgeryBiogenesisHumanJournal of proteome research
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Metal Ions and Metal Complexes in Alzheimer's Disease.

2015

Background: Alzheimer’s disease (AD) is the most common form of dementia that seriously affects daily life. Even if AD pathogenesis is still subject of debate, it is generally accepted that cerebral cortex plaques formed by aggregated amyloid-β (Aβ) peptides can be considered a characteristic pathological hallmark. It is well known that metal ions play an important role in the aggregation process of Aβ. Methods: This review focuses on the anti-Aβ aggregation activity of chelating ligands as well as on the use of metal complexes as diagnostic probes and as potential drugs. Conclusion: While chelating agents, such as curcumin or flavonoid derivatives, are currently used to capture metal ions …

0301 basic medicineStereochemistryMetal ions in aqueous solutionchemistry.chemical_elementProtein aggregationImagingPathogenesis03 medical and health scienceschemistry.chemical_compoundProtein AggregatesAlzheimer DiseaseCoordination ComplexesMetals HeavyDrug DiscoveryAD drugmedicineDementiaAnimalsHumansChelationMetal ionPharmacologyAmyloid beta-PeptidesDrug Discovery3003 Pharmaceutical ScienceAnti-aβ aggregating agentmedicine.diseaseCombinatorial chemistryRuthenium030104 developmental biologychemistrySettore CHIM/03 - Chimica Generale E InorganicaCurcuminMetal complexeAlzheimer's diseaseAlzheimer’s diseaseCurrent pharmaceutical design
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Structure and Synaptic Function of Metal Binding to the Amyloid Precursor Protein and its Proteolytic Fragments

2017

Alzheimer’s disease (AD) is ultimately linked to the Amyloid Precursor Protein (APP). However, current research reveals an important synaptic function of APP and APP-like proteins (APLP1 and 2). In this context various neurotrophic and neuroprotective functions have been reported for the APP proteolytic fragments sAPPα, sAPPβ, and the monomeric amyloid-beta peptide (Aβ). APP is a metalloprotein and binds copper and zinc ions. Synaptic activity correlates with a release of these ions into the synaptic cleft and dysregulation of their homeostasis is linked to different neurodegenerative diseases. Metal binding to APP or its fragments affects its structure and its proteolytic cleavage and ther…

0301 basic medicineSynaptic cleftamyloid precursor protein (APP)Context (language use)ReviewNeurotransmission03 medical and health sciencesCellular and Molecular Neurosciencemental disordersAmyloid precursor proteinsynaptic transmissionAPLP1Molecular BiologybiologyChemistryzincP3 peptideCell biologyBiochemistry of Alzheimer's disease030104 developmental biologyAlpha secretaseBiochemistrycopperbiology.proteinAlzheimer’s diseaseNeuroscienceFrontiers in Molecular Neuroscience
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