Search results for "Tau protein"

showing 10 items of 48 documents

Modulating disease-relevant tau oligomeric strains by small molecules

2020

The pathological aggregation of tau plays an important role in Alzheimer's disease and many other related neurodegenerative diseases, collectively referred to as tauopathies. Recent evidence has demonstrated that tau oligomers, small and soluble prefibrillar aggregates, are highly toxic due to their strong ability to seed tau misfolding and propagate the pathology seen across different neurodegenerative diseases. We previously showed that novel curcumin derivatives affect preformed tau oligomer aggregation pathways by promoting the formation of more aggregated and nontoxic tau aggregates. To further investigate their therapeutic potential, we have extended our studies o disease-relevant bra…

0301 basic medicinetau oligomeric strainsCurcuminTau proteinsmall moleculetau ProteinsProtein aggregationBiochemistrytau proteinoligomerProgressive supranuclear palsyprotein aggregationDiagnosis DifferentialSmall Molecule Libraries03 medical and health scienceschemistry.chemical_compoundBiopolymersmental disordersmedicineHumansMolecular BiologyCells CulturedNeurons030102 biochemistry & molecular biologybiologyChemistryDementia with Lewy bodiesbrain-derived tau oligomerstau aggregationtauopathytoxicityBrainMolecular Bases of DiseaseCell Biologymedicine.diseaseSmall moleculeImaging agentCell biology030104 developmental biologyTauopathiesbiology.proteinCurcuminTauopathyThe Journal of Biological Chemistry
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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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Alzheimer’s disease and infections, where we stand and where we go

2014

Editorial Alzheimer’s disease (AD) is a progressive neurological disorder, which represents the most common form of dementia, one of the major causes of disability in later life. Age is the greatest risk factor for AD, which typically affects people aged 65 years and over, with an age-standardised prevalence of 4.4 [1]. However, AD is not a normal part of ageing and advanced age alone does not justify the disease. Several pathways have been implicated in AD pathophysiology, the most described is the neurodegenerative one, which lead to the brain accumulation of beta-amyloid and neurofibrillary tangles, aggregations of hyperphosphorylated tau protein, macroscopically resulting in brain atrop…

AgingTraumatic brain injuryImmunologyTau proteinperiodontal diseaseDiseaseInfectionsBioinformaticsAtrophyAlzheimer'MedicineDementiaRisk factorAlzheimer's; infections; herpes viruses; periodontal disease; infectionInflammationSettore MED/04 - Patologia Generalebiologybusiness.industryVascular diseaseHerpes virusesOdds ratiomedicine.diseaseinfectionAgeingEditorialImmunologybiology.proteinherpes viruseSettore MED/26 - NeurologiabusinessAlzheimer’s diseaseImmunity & Ageing
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Biomarkers Related to Synaptic Dysfunction to Discriminate Alzheimer’s Disease from Other Neurological Disorders

2022

Recently, the synaptic proteins neurogranin (Ng) and α-synuclein (α-Syn) have attracted scientific interest as potential biomarkers for synaptic dysfunction in neurodegenerative diseases. In this study, we measured the CSF Ng and α-Syn concentrations in patients affected by AD (n = 69), non-AD neurodegenerative disorders (n-AD = 50) and non-degenerative disorders (n-ND, n = 98). The concentrations of CSF Ng and α-Syn were significantly higher in AD than in n-AD and n-ND. Moreover, the Aβ42/Ng and Aβ42/α-Syn ratios showed statistically significant differences between groups and discriminated AD patients from n-AD patients, better than Ng or α-Syn…

Alzheimer’s disease; biomarkers; neurogranin; α-synucleinAmyloid beta-PeptidesneurograninOrganic ChemistrybiomarkersNeurodegenerative Diseasestau ProteinsGeneral MedicineCatalysisSettore MED/01 - Statistica MedicaComputer Science ApplicationsInorganic Chemistryα-synucleinAlzheimer DiseaseFluorodeoxyglucose F18alpha-SynucleinHumansCognitive DysfunctionSettore MED/26 - NeurologiaPhysical and Theoretical ChemistryAlzheimer’s diseaseMolecular BiologySpectroscopyInternational Journal of Molecular Sciences; Volume 23; Issue 18; Pages: 10831
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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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GAL4-responsive UAS- tau as a tool for studying the anatomy and development of the Drosophila central nervous system

1997

To improve the quality of cytoplasmic labelling of GAL4-expressing cells in Drosophila enhancer-trap and transgenic strains, a new GAL4-responsive reporter UAS-tau, which features a bovine tau cDNA under control of a yeast upstream activation sequence (UAS), was tested. Tau, a microtubule-associated protein, is distributed actively and evenly into all cellular processes. Monoclonal anti-bovine Tau antibody reveals the axonal structure of the labelled cells with detail similar to that of Golgi impregnation. We demonstrate that the UAS-tau system is especially useful for studying processes of differentiation and reorganisation of identified neurones during postembryonic development.

Central Nervous SystemSaccharomyces cerevisiae ProteinsHistologyTransgenetau ProteinsBiologyProteomicsPathology and Forensic MedicineAnimals Genetically ModifiedFungal ProteinsUpstream activating sequenceGenes ReporterComplementary DNAmental disordersAnimalsEnhancer trapGenetic TestingTranscription factorNeuronsRegulation of gene expressionMetamorphosis BiologicalAntibodies MonoclonalGene Expression Regulation DevelopmentalCell BiologyAnatomyDNA-Binding ProteinsEnhancer Elements GeneticCytoplasmCattleDrosophilaTranscription FactorsCell and Tissue Research
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Curcumin-derived pyrazoles and isoxazoles: Swiss army knives or blunt tools for Alzheimer's disease?

2007

Curcumin binds to the amyloid beta peptide (Abeta) and inhibits or modulates amyloid precursor protein (APP) metabolism. Therefore, curcumin-derived isoxazoles and pyrazoles were synthesized to minimize the metal chelation properties of curcumin. The decreased rotational freedom and absence of stereoisomers was predicted to enhance affinity toward Abeta(42) aggregates. Accordingly, replacement of the 1,3-dicarbonyl moiety with isosteric heterocycles turned curcumin analogue isoxazoles and pyrazoles into potent ligands of fibrillar Abeta(42) aggregates. Additionally, several compounds are potent inhibitors of tau protein aggregation and depolymerized tau protein aggregates at low micromolar …

CurcuminMagnetic Resonance SpectroscopyAmyloid betaStereochemistryTau proteinPeptidetau ProteinsBiochemistrychemistry.chemical_compoundInhibitory Concentration 50Radioligand AssayAlzheimer Diseasemental disordersDrug DiscoveryAmyloid precursor proteinFluorescence Resonance Energy TransferMoietyAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsEnzyme InhibitorsCells CulturedCell ProliferationPharmacologychemistry.chemical_classificationAmyloid beta-PeptidesbiologyOrganic ChemistryP3 peptideIsoxazolesBiochemistrychemistrybiology.proteinCurcuminMolecular MedicinePyrazolesAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseChickensChemMedChem
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Diabetes and cognitive decline

2022

Epidemiologic studies have documented an association between diabetes and increased risk of cognitive decline in the elderly. Based on animal model studies, several mechanisms have been proposed to explain such an association, including central insulin signaling, neurodegeneration, brain amyloidosis, and neuroinflammation. Nevertheless, the exact mechanisms in humans remain poorly defined. It is reasonable, however, that many pathways may be involved in these patients leading to cognitive impairment. A major aim of clinicians is identifying early onset of neurologic signs and symptoms in elderly diabetics to improve quality of life of those with cognitive impairment and reduce costs associa…

Diabetes mellituAmyloid beta-Peptidestau ProteinsAmyloid beta-peptideBiomarkerAmyloidosisVascular dementiaSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaDiabetes mellitusGlycated hemoglobinSettore MED/13Alzheimer DiseaseTau proteinQuality of LifeBlood glucoseHumansDementiaCognitive DysfunctionBiomarkersRisk assessmentAged
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Aβ and tau toxicities in Alzheimer’s are linked via oxidative stress-induced p38 activation: Protective role of vitamin E

2014

AbstractOxidative stress is a hallmark of Alzheimer’s disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E).We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 …

Genetically modified mouseMalemedicine.medical_specialtyCell signalingAntioxidantP-p38p38 mitogen-activated protein kinasesmedicine.medical_treatmentClinical BiochemistryMice Transgenictau ProteinsBiologyBeta-amyloidmedicine.disease_causeProtective AgentsBiochemistryHippocampusp38 Mitogen-Activated Protein KinasesArticlechemistry.chemical_compoundMiceAlzheimer DiseaseInternal medicinemental disordersmedicineVitamin EAnimalsPhosphorylationlcsh:QH301-705.5Cells CulturedNeuronslcsh:R5-920Amyloid beta-PeptidesVitamin EOrganic Chemistrymedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologylcsh:Biology (General)chemistryTroloxAlzheimer's diseaseAntioxidantlcsh:Medicine (General)Oxidative stressRedox Biology
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Physical exercise in the prevention and treatment of Alzheimer's disease

2020

Highlights • Low levels of physical activity are a risk factor associated with Alzheimer's disease. • Older adults who exercise are more likely to maintain cognition. • Exercise modulates amyloid β turnover, inflammation, synthesis, and release of neurotrophins, and cerebral blood flow.

GerontologyAgingPsychological interventionPhysical Therapy Sports Therapy and RehabilitationPhysical exercisetau ProteinsDiseaseReviewLifestyle factorsExercise traininglcsh:GV557-1198.99503 medical and health sciences0302 clinical medicineCognitionAlzheimer DiseaseRisk FactorsmedicineDementiaAerobic exerciseAnimalsHumansOrthopedics and Sports Medicine030212 general & internal medicineHealthy LifestyleNerve Growth Factorslcsh:Sports medicineExerciseAerobic exerciselcsh:SportsInflammationAmyloid beta-Peptidesbusiness.industryMechanism (biology)BrainMultidomain interventionsCognition030229 sport sciencesmedicine.diseaseMental healthResistance exercise3. Good healthExercise TherapyCerebrovascular CirculationDementialcsh:RC1200-1245business[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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