Search results for "Alzheimer Disease"

showing 10 items of 428 documents

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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Collapsibility of the internal jugular veins in the lateral decubitus body position: A potential protective role of the cerebral venous outflow again…

2019

Recent research has revealed that patients with neurodegenerative disease sleep longer in the supine position, while healthy controls prefer sleeping in the lateral decubitus position. Thus, sleeping in the lateral position seems to be protective against neurodegeneration. It has also been suggested that a protective role of this body position could be associated with better cerebral venous drainage in this body position, which results in more active glymphatic system of the brain (the system responsible for clearance of the cerebral tissue from waste products, e.g. amyloid-β). Since no published evidence exists regarding venous outflow from the cranial cavity in the lateral decubitus posit…

0301 basic medicineSupine positionModels NeurologicalPostureBlood PressurePilot ProjectsLateral decubitus positionSitting03 medical and health sciencesHabits0302 clinical medicineAlzheimer DiseaseReference Valuesmental disordersCranial cavitymedicineLateral Decubitus PositionSupine PositionHumansNeurodegenerationInternal jugular veinhealth care economics and organizationsUltrasonographyRight Lateral Decubitus PositionAquaporin 4business.industryNeurodegenerationHemodynamicsGeneral MedicineAnatomyAlzheimer's diseasemedicine.diseaseCerebral Veins030104 developmental biologymedicine.anatomical_structureCerebrovascular CirculationPulsatile FlowNerve Degenerationcardiovascular systemInternal jugular veinGlymphatic systemJugular VeinsbusinessSleepGlymphatic System030217 neurology & neurosurgeryBlood Flow VelocityMedical hypotheses
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Azure C Targets and Modulates Toxic Tau Oligomers.

2018

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder affecting millions of people worldwide. Therefore, finding effective interventions and therapies is extremely important. AD is one of over 20 different disorders known as tauopathies, characterized by the pathological aggregation and accumulation of tau, a microtubule-associated protein. Tau aggregates are heterogeneous and can be divided into two major groups: large metastable fibrils, including neurofibrillary tangles, and oligomers. The smaller, soluble and dynamic tau oligomers have been shown to be more toxic with more proficient seeding properties for the propagation of tau pathology as compared to the …

0301 basic medicineTau pathologyPhysiologyCognitive Neurosciencetau ProteinsFibrilBiochemistryOligomerAzure Stains03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEffective interventionsAlzheimer DiseaseCell Line TumorHumansNeurofibrillary TanglesCell BiologyGeneral MedicineSmall molecule030104 developmental biologychemistryTauopathiesBiophysicsPaired helical filamentsDisease Progression030217 neurology & neurosurgeryACS chemical neuroscience
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Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer’s disease

2018

Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or …

0301 basic medicineTime Factorsmedicine.medical_treatmentHippocampusCell CountPharmacologymedicine.disease_causeHippocampuslcsh:RC346-429Superoxide Dismutase-10302 clinical medicineNeuroinflammationNF-kBMicrogliaGeneral NeuroscienceMicrofilament ProteinsROSPro-inflammatory cytokineIFNβ1amedicine.anatomical_structureCytokineNeurologyIL-10CytokinesFemalemedicine.symptomAlzheimer's diseaseInterferon beta-1aPro-inflammatory cytokinesImmunologyAβ 1-42InflammationProinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceHippocampuAlzheimer DiseaseGlial Fibrillary Acidic ProteinmedicineAnimalsAβ1-42Rats WistarSODMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationInflammationAmyloid beta-PeptidesNeuroscience (all)Superoxide Dismutasebusiness.industryResearchCalcium-Binding ProteinsRecognition Psychologymedicine.diseasePeptide FragmentsRatsDisease Models Animal030104 developmental biologyLipid PeroxidationCognition DisordersReactive Oxygen Speciesbusiness030217 neurology & neurosurgeryOxidative stressJournal of Neuroinflammation
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Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC

2019

Seventy years of research on Western Pacific amyotrophic lateral sclerosis and Parkinsonism-dementia Complex (ALS/PDC) have provided invaluable data on the etiology, molecular pathogenesis and latency of this disappearing, largely environmental neurodegenerative disease. ALS/PDC is linked to genotoxic chemicals (notably methylazoxymethanol, MAM) derived from seed of the cycad plant (Cycas spp.) that were used as a traditional food and/or medicine in all three disease-affected Western Pacific populations. MAM, nitrosamines and hydrazines generate methyl free radicals that damage DNA (in the form of O6-methylguanine lesions) that can induce mutations in cycling cells and degenerative changes …

0301 basic medicineamyotrophic lateral sclerosisDNA damageDiseaseBiologylcsh:RC346-429Environmental - originProgressive supranuclear palsy03 medical and health sciences0302 clinical medicineHypothesis and TheorymedicinenitrosaminesAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemhydrazinesprogressive supranuclear palsymedicine.diseaseatypical parkinsonism030104 developmental biologyBrain degenerationNeurologyImmunologyEtiologycycad methylazoxymethanol and L-BMAADNA damageNeurology (clinical)Alzheimer's diseaseAlzheimer disease030217 neurology & neurosurgeryFrontiers in Neurology
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Dysregulation of C-X-C motif ligand 10 during aging and association with cognitive performance

2017

International audience; Chronic low-grade inflammation during aging (inflammaging) is associated with cognitive decline and neurodegeneration; however, the mechanisms underlying inflammaging are unclear. We studied a population (n = 361) of healthy young and old adults from the MyoAge cohort. Peripheral levels of C-X-C motif chemokine ligand 10 (CXCL10) was found to be higher in older adults, compared with young, and negatively associated with working memory performance. This coincided with an age-related reduction in blood DNA methylation at specific CpGs within the CXCL10 gene promoter. In vitro analysis supported the role of DNA methylation in regulating CXCL10 transcription. A polymorph…

0301 basic medicinegamma interferon inducible protein 10genomic DNAAlzheimerin tautiEpigenesis GeneticCohort StudiesCXCL10 geneCognitionsingle nucleotide polymorphismcognitive defectCognitive declineAged 80 and overCerebral Cortexeducation.field_of_studyprefrontal cortexDNA methylationGeneral NeuroscienceadultNeurodegenerationneurodegenerationta3141U937 CellsMethylationta3142Alzheimer's diseasecohort analysisDNA-metylaatioagedfemalepriority journalepigenetiikkaDNA methylationAlzheimer's diseaseAlzheimer diseasetranscription regulationAlzheimer’s diseasekognitiiviset taidotmedicine.medical_specialty[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]in vitro studyAdolescentheredityPopulationBiologyArticleworking memoryYoung Adult03 medical and health sciencesCognitive agingpromoter regionmaleMemoryInternal medicineJournal Articlemedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansCXCL10controlled studyEpigeneticshumanbrain levelNeurodegenerationeducationepigeneticscognitive aginghuman cellagingdisease associationmedicine.diseasemajor clinical studyInflammagingChemokine CXCL10gamma interferon inducible protein 10; genomic DNA adult; age; aged; aging; Alzheimer disease; Article; brain level; cognitive defect; cohort analysis; controlled study; CpG island; CXCL10 gene; disease association; DNA methylation; epigenetics; female; heredity; human; human cell; in vitro study; inflammation; major clinical study; male; prefrontal cortex; priority journal; promoter region; single nucleotide polymorphism; transcription regulation; working memory; Alzheimer's disease; Cognitive aging; DNA methylation; Epigenetics; Inflammaging; Neurodegeneration030104 developmental biologyEndocrinologyikääntyminenageinflammationNerve DegenerationCpG islandinflammagingNeurology (clinical)Geriatrics and GerontologyHeLa CellsDevelopmental BiologyNeurobiology of Aging
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Heat Shock Proteins in Alzheimer’s Disease: Role and Targeting

2018

Among diseases whose cure is still far from being discovered, Alzheimer’s disease (AD) has been recognized as a crucial medical and social problem. A major issue in AD research is represented by the complexity of involved biochemical pathways, including the nature of protein misfolding, which results in the production of toxic species. Considering the involvement of (mis)folding processes in AD aetiology, targeting molecular chaperones represents a promising therapeutic perspective. This review analyses the connection between AD and molecular chaperones, with particular attention toward the most important heat shock proteins (HSPs) as representative components of the human chaperome: Hsp60,…

0301 basic medicineheat shock proteinDiseaseReviewprotein TauHsp70lcsh:ChemistrychaperoneEnzyme Inhibitorslcsh:QH301-705.5SpectroscopybiologyGeneral MedicineHsp60Hsp90Computer Science Applicationsamyloid peptideModels AnimalHSP60Protein foldingAlzheimer’s diseaseheat shock proteins; chaperones; Alzheimer’s disease; amyloid peptide; protein Tau; Hsp60; Hsp70; Hsp90Tau proteintau ProteinsHsp90Computational biologyCatalysisInorganic ChemistryMitochondrial Proteins03 medical and health sciencesAlzheimer DiseaseHeat shock proteinAnimalsHumanschaperonesHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsPhysical and Theoretical ChemistryMolecular BiologyAmyloid beta-PeptidesSettore BIO/16 - Anatomia UmanaOrganic ChemistryChaperonin 60Settore CHIM/06 - Chimica OrganicaHsp70030104 developmental biologylcsh:Biology (General)lcsh:QD1-999heat shock proteinsbiology.protein
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Alzheimer's disease: Only prevention makes sense

2018

Alzheimer's disease therapeutics is one of the most important endeavours in today's clinical investigation. Over more than 30 years of research, no disease-modifying treatment has been approved by either the FDA or the EMA to treat Alzheimer's disease. Recently, the evidence of pathological alterations in the brain tissue has been gathered showing that the signs of brain damage appear more than 20 years before the onset of Alzheimer's dementia. The major aim of this review is to underpin the idea that in Alzheimer's therapeutics, only prevention makes sense. It is difficult to visualise that would-be patients may be treated with endovenous administration of antibodies for several years to d…

0301 basic medicinemedicine.medical_specialtyClinical BiochemistryBrain damageDiseaseBiochemistryAsymptomaticAntioxidantsMice03 medical and health sciences0302 clinical medicineAlzheimer DiseaseAnimalsHumansVitamin EMedicineDementiaHealthy LifestyleTreatment FailureIntensive care medicinePathologicalNootropic AgentsAgedAged 80 and overClinical Trials as Topicbusiness.industryAntibodies MonoclonalCognitionGeneral MedicineMiddle Agedmedicine.diseaseClinical trialDisease Models Animal030104 developmental biologymedicine.symptombusiness030217 neurology & neurosurgeryMinimal cognitive impairmentEuropean Journal of Clinical Investigation
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Olesoxime improves cerebral mitochondrial dysfunction and enhances Aβ levels in preclinical models of Alzheimer's disease.

2019

Abstract Background Approved drugs for Alzheimer's disease (AD) only have a symptomatic effects and do not intervene causally in the course of the disease. Olesoxime (TRO19622) has been tested in AD disease models characterized by improved amyloid precursor protein processing (AβPP) and mitochondrial dysfunction. Methods Three months old Thy-1-AβPPSL (tg) and wild type mice (wt) received TRO19622 (100 mg/kg b.w.) in supplemented food pellets for 15 weeks (tg TRO19622). Mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) levels were determined in dissociated brain cells (DBC). Respiration was analyzed in mitochondria isolated from brain tissue. Citrate synthase (CS) activ…

0301 basic medicinemedicine.medical_specialtyRespiratory chainMice TransgenicMitochondrionLipid peroxidation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeuroscienceAlzheimer DiseaseInternal medicineMembrane fluidityAmyloid precursor proteinmedicineCitrate synthaseAnimalsHumansCholestenonesAmyloid beta-PeptidesbiologyBrainRotenoneMitochondriaMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyHEK293 CellsNeurologychemistrybiology.proteinOlesoximeFemale030217 neurology & neurosurgeryExperimental neurology
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When Does Alzheimer′s Disease Really Start? The Role of Biomarkers

2021

While Alzheimer’s disease (AD) classical diagnostic criteria rely on clinical data from a stablished symptomatic disease, newer criteria aim to identify the disease in its earlier stages. For that, they incorporated the use of AD’s specific biomarkers to reach a diagnosis, including the identification of Aβ and tau depositions, glucose hypometabolism, and cerebral atrophy. These biomarkers created a new concept of the disease, in which AD’s main pathological processes have already taken place decades before we can clinically diagnose the first symptoms. Therefore, AD is now considered a dynamic disease with a gradual progression, and dementia is its final stage. With …

0301 basic medicinemedicine.medical_specialtyad spectrumGradual progressionVariable timeInfluential PublicationsReviewDiseaseCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineAlzheimer DiseaseRisk FactorsmedicineHumansDementiaPhysical and Theoretical ChemistryIntensive care medicineCognitive impairmentlcsh:QH301-705.5Molecular BiologyPathologicalad dynamicimaging biomarkersSpectroscopyCerebral atrophybusiness.industryOrganic ChemistrybiomarkerscsfGeneral Medicinemedicine.diseaseComputer Science Applications030104 developmental biologylcsh:Biology (General)lcsh:QD1-999business030217 neurology & neurosurgerydementiaInternational Journal of Molecular Sciences
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