Search results for "AMYLOID"

showing 10 items of 494 documents

Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer's disease: histotopographical correlation with amyloid pl…

1999

Impairment of cholinergic transmission and decreased numbers of nicotinic binding sites are well-known features accompanying the cognitive dysfunction seen in Alzheimer's disease (AD). In order to elucidate the underlying cause of this cholinoceptive dysfunction, the expression of two pharmacologically different nicotinic acetylcholine receptor (nAChR) subunits (alpha4, alpha7) was studied in the cerebral cortex of Alzheimer patients as compared to controls. Patch-clamp recordings of 14 dissociated neurons of control cortices showed responses suggesting the existence of alpha4- and alpha7-containing functional nAChRs in the human cortex. In cortices of Alzheimer patients and controls, the p…

MaleAmyloidTau proteinPlaque Amyloidtau ProteinsReceptors Nicotiniccomplex mixturesAlzheimer DiseaseCortex (anatomy)mental disordersmedicineHumansProtein IsoformsRNA MessengerPhosphorylationAgedAged 80 and overCerebral CortexNeuronsAmyloid beta-PeptidesbiologyGeneral NeuroscienceHuman brainFrontal LobeNicotinic acetylcholine receptormedicine.anatomical_structureNicotinic agonistnervous systemCerebral cortexbiology.proteinCholinergicFemalesense organsNeuroscienceEuropean Journal of Neuroscience
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Effect of gender on mitochondrial toxicity of Alzheimer's Abeta peptide.

2007

The aim of this article is to review the role of mitochondria in the pathogenesis of Alzheimer's disease. Additionally, the effect of gender on the incidence of Alzheimer's disease and the pathophysiological mechanisms involved will be discussed. Mitochondria, in the presence of Alzheimer's amyloid-beta peptide, increase the formation of reactive oxygen species which act both as damaging agents and also as signaling molecules. These radicals, in fact, unleash a mechanism involving the liberation of cytochrome c that leads to neuronal apoptosis. Notably, young females appear protected against the mitochondrial toxicity of amyloid-beta, likely due to the upregulation of antioxidant enzymes wh…

MaleAntioxidantPhysiologymedicine.medical_treatmentClinical BiochemistryPharmacologyMitochondrionBiologymedicine.disease_causeBiochemistryp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundDownregulation and upregulationAlzheimer DiseasemedicineHumansMolecular BiologyGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesAmyloid beta-PeptidesEstrogensCell Biologymedicine.diseaseOxidantsMitochondriaEnzyme ActivationMitochondrial toxicitychemistryBiochemistryToxicityGeneral Earth and Planetary SciencesPhytoestrogensFemaleOxidative stressAntioxidantsredox signaling
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Apolipoprotein E isoforms and the development of low and high Braak stages of Alzheimer's disease-related lesions

1999

In recent research, apolipoprotein-E (apoE) polymorphism has been shown to influence the formation of neurofibrillary changes and the accumulation of beta/A4-amyloid, the histopathological hallmarks of Alzheimer's disease (AD). Clinical studies associate the apoE allele epsilon4 with earlier onset of the disease, although the clinical speed of progression remains unchanged. Time course estimates have also provided evidence which indicates that the clinical phase of AD constitutes only 10-20% of the total time span needed for the development of this slowly progressing degenerative brain disorder. Due to the lack of reliable clinical tests for the detection of pre-symptomatic stages of AD, we…

MaleApolipoprotein Emedicine.medical_specialtyPathologyGenotypeApolipoprotein BApolipoprotein E2Apolipoprotein E4Apolipoprotein E3tau ProteinsNeuropathologyPathology and Forensic MedicineCellular and Molecular NeuroscienceApolipoproteins EDegenerative diseaseIsomerismAlzheimer DiseaseInternal medicineGenotypemedicineHumansAlleleAllelesBrain ChemistryAmyloid beta-PeptidesPolymorphism GeneticbiologyBrainNeurofibrillary TanglesNeurofibrillary tangleMiddle Agedmedicine.diseaseEndocrinologyDisease Progressionbiology.proteinFemaleNeurology (clinical)Alzheimer's diseaseActa Neuropathologica
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Glia talk back.

2014

This study shows that the activity of neurons can trigger shedding of a protein, NG2, from the surface of oligodendrocyte precursor cells; this protein in turn modulates synaptic transmission, revealing a two-way conversation between neurons and glia.

MaleCell signalingNeural NetworksQH301-705.5AMPA receptorBiologyNeurotransmissionResearch and Analysis MethodsMechanical Treatment of SpecimensGeneral Biochemistry Genetics and Molecular BiologyBehavioral NeuroscienceNeurotransmitter receptormedicineBiological neural networkPremovement neuronal activityAnimalsBiology (General)AntigensNeuronsGeneral Immunology and MicrobiologyGeneral NeuroscienceMembrane ProteinsBiology and Life SciencesLong-term potentiationADAM ProteinsOligodendrogliamedicine.anatomical_structureElectroporationnervous systemSpecimen DisruptionSpecimen Preparation and TreatmentCellular NeuroscienceImmunologyProteoglycansNeuronAmyloid Precursor Protein SecretasesMolecular NeuroscienceGeneral Agricultural and Biological SciencesNeuroscienceResearch ArticleNeurosciencePLoS biology
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Increased CSF APPs-  levels in patients with Alzheimer disease treated with acitretin

2014

Objective: We investigated induction of α-secretase A disintegrin and metalloprotease 10 (ADAM10) by the synthetic retinoid acitretin (Neotigason; Actavis, Munchen-Riem, Germany) in patients with mild to moderate Alzheimer disease (AD) via measurement of CSF content of α-secretase–derived amyloid precursor protein (APPs-α). Methods: Twenty-one patients clinically diagnosed with mild to moderate AD received acitretin (30 mg per day) or placebo in a 4-week double-blind study. Primary endpoint was the difference of CSF APPs-α ratios calculated from the APPs-α levels after treatment and at baseline. We monitored safety and tolerability of the treatment. In addition, we assessed biomarkers such …

MaleDrugmedicine.medical_specialtymedia_common.quotation_subjectPilot ProjectsPlaceboGastroenterologyAcitretinlaw.inventionDouble-Blind MethodRandomized controlled trialAlzheimer Diseasecerebrospinal fluid [Amyloid Precursor Protein Secretases]lawInternal medicinemedicineClinical endpointdrug therapy [Alzheimer Disease]Humansddc:610Prospective StudiesProspective cohort studyAgedmedia_commonbusiness.industrytherapeutic use [Acitretin]diagnosis [Alzheimer Disease]Middle Agedmedicine.diseaseAcitretincerebrospinal fluid [Alzheimer Disease]Treatment Outcomecerebrospinal fluid [Biomarkers]TolerabilityFemaleNeurology (clinical)Amyloid Precursor Protein SecretasesAlzheimer's diseasebusinessBiomarkersmedicine.drugNeurology
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Systemic Immune Responses in Alzheimer's Disease: In Vitro Mononuclear Cell Activation and Cytokine Production

2010

To investigate the systemic signs of immune-inflammatory responses in Alzheimer's disease (AD), in the present study we have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells (PBMCs) from AD patients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-beta peptide (rAbeta42). Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage of B cells when compared to HC lymphocytes, whereas the other subsets are not significantly different in patients and controls. We report the increased expression of the activation marker CD69 and of the chemoki…

MaleEotaxinCCR2ChemokineTime Factorsmedicine.medical_treatmentPeripheral blood mononuclear cellChemokine receptorImmune systemAlzheimer’s disease chemokine cytokine PBMC rAβ42Alzheimer DiseasemedicineHumansLymphocytesIL-2 receptorCells CulturedAgedSettore MED/04 - Patologia GeneraleAged 80 and overAnalysis of VarianceAmyloid beta-Peptidesbiologybusiness.industryGeneral NeuroscienceGeneral MedicineMiddle AgedFlow CytometryPeptide FragmentsPsychiatry and Mental healthClinical PsychologyCytokineGene Expression RegulationCase-Control StudiesImmunologyLeukocytes Mononuclearbiology.proteinCytokinesFemaleGeriatrics and GerontologybusinessJournal of Alzheimer's Disease
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The Anti-amyloid Compound DO1 Decreases Plaque Pathology and Neuroinflammation-Related Expression Changes in 5xFAD Transgenic Mice

2018

Self-propagating amyloid-β (Aβ) aggregates or seeds possibly drive pathogenesis of Alzheimer's disease (AD). Small molecules targeting such structures might act therapeutically in vivo. Here, a fluorescence polarization assay was established that enables the detection of compound effects on both seeded and spontaneous Aβ42 aggregation. In a focused screen of anti-amyloid compounds, we identified Disperse Orange 1 (DO1) ([4-((4-nitrophenyl)diazenyl)-N-phenylaniline]), a small molecule that potently delays both seeded and non-seeded Aβ42 polymerization at substoichiometric concentrations. Mechanistic studies revealed that DO1 disrupts preformed fibrillar assemblies of synthetic Aβ42 peptides …

MaleGenetically modified mouse1303 BiochemistryAmyloid10017 Institute of AnatomyClinical BiochemistryMice TransgenicPlaque Amyloid610 Medicine & healthBiologyProtein aggregation1308 Clinical Biochemistry01 natural sciencesBiochemistryPolymerizationPathogenesisMiceProtein AggregatesStructure-Activity RelationshipAlzheimer DiseaseGene expressionDrug Discovery1312 Molecular BiologyAnimalsColoring AgentsMolecular BiologyNeuroinflammationInflammationPharmacologyAmyloid beta-PeptidesDose-Response Relationship DrugMolecular Structure010405 organic chemistry3002 Drug DiscoveryBrainSmall moleculeMolecular medicine0104 chemical sciencesCell biologyMice Inbred C57BL3004 Pharmacology10036 Medical Clinic1313 Molecular Medicine570 Life sciences; biologyMolecular MedicineFemaleAzo Compounds
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Acitretin, an Enhancer of Alpha-Secretase Expression, Crosses the Blood-Brain Barrier and Is Not Eliminated by P-Glycoprotein

2011

<i>Background:</i> ADAM10 (a disintegrin and metalloproteinase 10) has been demonstrated to act as the main physiological α-secretase. Enzymatic activity of the α-secretase on the one hand prevents the formation of toxic Aβ peptides and on the other hand promotes the secretion of a neurotrophic and neuroprotective amyloid precursor protein fragment (APPs-α) by cleaving the amyloid precursor protein within its Aβ sequence. Enhancement of ADAM10’s gene expression may therefore present a valuable therapeutic approach for the treatment of Alzheimer’s disease (AD), where Aβ peptides are severely involved in the pathogenesis. <i>Objective:</i> In cell culture and in a tran…

MaleGenetically modified mouseATP Binding Cassette Transporter Subfamily BTime FactorsADAM10PharmacologyTransfectionAcitretinADAM10 ProteinMiceNeuroblastomachemistry.chemical_compoundCell Line TumormedicineAmyloid precursor proteinAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1Chromatography High Pressure LiquidP-glycoproteinMice KnockoutAnalysis of VarianceReporter genebiologyMembrane ProteinsMolecular biologyAcitretinADAM ProteinsGene Expression RegulationNeurologychemistryAlpha secretaseBlood-Brain Barrierbiology.proteinTamibaroteneNeurology (clinical)Amyloid Precursor Protein Secretasesmedicine.drugNeurodegenerative Diseases
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Low-Density Lipoprotein Receptor-Related Protein 8 at the Crossroad between Cancer and Neurodegeneration

2022

The low-density-lipoprotein receptors represent a family of pleiotropic cell surface receptors involved in lipid homeostasis, cell migration, proliferation and differentiation. The family shares common structural features but also has significant differences mainly due to tissue-specific interactors and to peculiar proteolytic processing. Among the receptors in the family, recent studies place low-density lipoprotein receptor-related protein 8 (LRP8) at the center of both neurodegenerative and cancer-related pathways. From one side, its overexpression has been highlighted in many types of cancer including breast, gastric, prostate, lung and melanoma; from the other side, LRP8 has a potentia…

MaleLRP8Organic ChemistryapolipoproteinGeneral MedicineAlzheimer's diseaseCatalysisLDL receptor familyComputer Science ApplicationsInorganic ChemistryLipoproteins LDLReceptors LDLAlzheimer DiseaseNeoplasmsHumanscancerPhysical and Theoretical ChemistryAmyloid Precursor Protein SecretasesLRP8; cancer; Alzheimer's disease; apolipoprotein; LDL receptor familyAlzheimer’s diseaseMolecular BiologySpectroscopyLow Density Lipoprotein Receptor-Related Protein-1
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Posttranslational modifications by ADAM10 shape myeloid antigen-presenting cell homeostasis in the splenic marginal zone

2021

The spleen contains phenotypically and functionally distinct conventional dendritic cell (cDC) subpopulations, termed cDC1 and cDC2, which each can be divided into several smaller and less well-characterized subsets. Despite advances in understanding the complexity of cDC ontogeny by transcriptional programming, the significance of posttranslational modifications in controlling tissue-specific cDC subset immunobiology remains elusive. Here, we identified the cell-surface–expressed A-disintegrin-and-metalloproteinase 10 (ADAM10) as an essential regulator of cDC1 and cDC2 homeostasis in the splenic marginal zone (MZ). Mice with a CD11c-specific deletion of ADAM10 (ADAM10(ΔCD11c)) exhibited a …

MaleLangerinLymphoid TissueNotch signaling pathwayAntigen-Presenting CellsCD11cSpleenADAM10 ProteinMicePhosphatidylinositol 3-KinasesmedicineAnimalsHomeostasisMyeloid CellsProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinarybiologyMacrophagesMembrane ProteinsCell DifferentiationDendritic CellsBiological SciencesCD11c AntigenCell biologyMice Inbred C57BLmedicine.anatomical_structurebiology.proteinFemaleAmyloid Precursor Protein SecretasesSignal transductionProtein Processing Post-TranslationalSpleenConventional Dendritic CellSignal TransductionProceedings of the National Academy of Sciences
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