Search results for "DEGENERATION"

showing 10 items of 601 documents

The antioxidant 2,3‐dichloro,5,8‐dihydroxy,1,4‐naphthoquinone inhibits acetyl‐cholinesterase activity and amyloid β 42 aggregation: A dual target the…

2020

Alzheimer's disease is characterized by amyloid β aggregation and cholinergic neurodegeneration. In the present study, pure DDN (2,3-dichloro-5,8-dihydroxy-1,4-naphthoquinone) was examined, for the first time, for its dual potential as inhibitor of acetylcholinesterase (AChE) and Aβ42 aggregation. Such investigation was encouraged by the in vitro high antioxidant potential of DDN. Indeed, it revealed interesting antioxidant activity with IC50 values of 9.8 and 4.3 µM for ABTS and reducing power, respectively. The ability of DDN to counteract Aβ42 aggregation was evaluated by thioflavine-T assay. Strong inhibition of Aβ42 aggregation of more than 90% at 25 µM was measured. Moreover, results …

0106 biological sciencesAntioxidantAchémedicine.medical_treatmentBiomedical EngineeringBioengineering14-Naphthoquinone01 natural sciencesApplied Microbiology and Biotechnology03 medical and health scienceschemistry.chemical_compound010608 biotechnologyDrug DiscoverymedicineIC50030304 developmental biology0303 health sciencesABTSChemistryProcess Chemistry and TechnologyNeurodegenerationGeneral Medicinemedicine.diseaseAcetylcholinesteraselanguage.human_languageIn vitroBiochemistrylanguageMolecular MedicineBiotechnologyBiotechnology and Applied Biochemistry
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Genetics of Wilson disease and Wilson-like phenotype in a clinical series from eastern Spain.

2019

Wilson's disease (WD) is an autosomal recessive disorder caused by ATP7B mutations. Subjects with only one mutation may show clinical signs and individuals with biallelic changes may remain asymptomatic. We aimed to achieve a conclusive genetic diagnosis for 34 patients clinically diagnosed of WD. Genetic analysis comprised from analysis of exons to WES (whole exome sequencing), including promoter, introns, UTRs (untranslated regions), besides of study of large deletions/duplications by MLPA (multiplex ligation-dependent probe amplification). Biallelic ATP7B mutations were identified in 30 patients, so that four patients were analyzed using WES. Two affected siblings resulted to be compound…

0301 basic medicineAdultMaleNerve Tissue Proteins030105 genetics & heredityBiologymedicine.disease_causeCompound heterozygosityGenetic analysis03 medical and health sciencesExonHepatolenticular DegenerationExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseMultiplex ligation-dependent probe amplificationGenetic TestingGenetics (clinical)Exome sequencingGeneticsMutationExonsmedicine.diseaseWilson's disease030104 developmental biologyPhenotypeCopper-Transporting ATPasesSpainMutationFemaleCongenital disorder of glycosylationClinical geneticsREFERENCES
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Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans

2017

Autophagy is a ubiquitous catabolic process that causes cellular bulk degradation of cytoplasmic components and is generally associated with positive effects on health and longevity. Inactivation of autophagy has been linked with detrimental effects on cells and organisms. The antagonistic pleiotropy theory postulates that some fitness-promoting genes during youth are harmful during aging. On this basis, we examined genes mediating post-reproductive longevity using an RNAi screen. From this screen, we identified 30 novel regulators of post-reproductive longevity, including pha-4. Through downstream analysis of pha-4, we identified that the inactivation of genes governing the early stages of…

0301 basic medicineAgingCytoplasmmedia_common.quotation_subjectLongevityVesicular Transport ProteinsContext (language use)Biology03 medical and health sciences0302 clinical medicinePleiotropyAutophagyGeneticsmedicineAnimalsGene SilencingCaenorhabditis elegansCaenorhabditis elegans ProteinsGenemedia_commonNeuronsGeneticsReproductionNeurodegenerationAutophagyLongevityGenetic Pleiotropymedicine.diseaseCell biology030104 developmental biologyCytoplasmSarcopeniaTrans-ActivatorsRNA InterferenceFunction and Dysfunction of the Nervous System030217 neurology & neurosurgerySignal TransductionResearch PaperDevelopmental BiologyGenes & Development
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The close link between the fetal programming imprinting and neurodegeneration in adulthood: The key role of “hemogenic endothelium” programming

2021

The research on neurodegenerative diseases (NeuroDegD) has been traditionally focused on later life stages. There is now an increasing evidence, that they may be programmed during early development. Here, we propose that NeuroDegD are the result of the complex process of imprinting on fetal hemogenic endothelium, from which the microglial cells make to origin. The central role of placenta and epigenetic mechanisms (methylation of DNA, histone modifications and regulation by non-coding RNAs) in mediating the short and long-term effects has been also described. Precisely, it reports their role in impacting plasticity and memory of microglial cells. In addition, we also underline the necessity…

0301 basic medicineAgingHemangioblastsCell PlasticityRisk AssessmentEpigenesis GeneticFetal DevelopmentMolecular Imprinting03 medical and health sciences0302 clinical medicineEpigenetic factors as biomarkers Sex dimorphism Fetal developmental programming Hemogenic endothelium Microglia plasticity and memory Neurodegenerative diseasesmedicineHumansSettore MED/05 - Patologia ClinicaEpigeneticsFetal programmingImprinting (organizational theory)Hemogenic endotheliumSex CharacteristicsBiological Variation Individualbiologybusiness.industryNeurodegenerationGene Expression Regulation DevelopmentalNeurodegenerative Diseasesmedicine.diseaseLife stage030104 developmental biologyHistonePrenatal stressbiology.proteinMicrogliabusinessNeuroscienceBiomarkers030217 neurology & neurosurgeryDevelopmental BiologyMechanisms of Ageing and Development
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Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative

2018

Microglial activation has been considered a crucial player in the pathological process of multiple human neurodegenerative diseases. In some of these pathologies, such as Amyotrophic Lateral Sclerosis or Multiple Sclerosis, the immune system and microglial cells (as part of the cerebral immunity) play a central role. In other degenerative processes, such as Alzheimer’s disease (AD), the role of microglia is far to be elucidated. In this “mini-review” article, we briefly highlight our recent data comparing the microglial response between amyloidogenic transgenic models, such as APP/PS1 and AD patients. Since the AD pathology could display regional heterogeneity, we focus our work at the hipp…

0301 basic medicineAgingMini ReviewCognitive NeuroscienceAPP modelsmicrogliainflamationDegeneration (medical)Hippocampal formationlcsh:RC321-57103 medical and health sciences0302 clinical medicineImmune systemmedicineAmyotrophic lateral sclerosislcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMicrogliabusiness.industryMultiple sclerosisDentate gyrusmedicine.disease030104 developmental biologymedicine.anatomical_structureAbeta plaquesMicrogliaAlzheimer diseaseAlzheimer's diseasebusinessInflamationNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Aging Neuroscience
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Differential Associations of IL-4 With Hippocampal Subfields in Mild Cognitive Impairment and Alzheimer’s Disease

2019

Background/Aims: A bi-directional communication between the immune system and the central nervous system has been recently suggested. Among many cytokines, the role of IL-4 - with anti-inflammatory properties- in counteracting age-related inflammatory changes in the brain is strongly supported among studies. With this study, we aimed at investigating the association between volumetric measures of hippocampal subregions -in healthy older controls (HC), subjects affected by mild cognitive impairment (MCI) and Alzheimer’s Disease (AD)- with circulating levels of IL-4. Methods: From AddNeuroMed Project 113 HC, 101 stable MCI (sMCI), 22 converter MCI (cMCI) and 119 AD were included. Hippocampal …

0301 basic medicineAgingmedicine.medical_specialtyCognitive NeuroscienceCentral nervous systemHippocampusInflammationDiseaseHippocampal formationNeuroprotectionAlzheimer’s disease; aging; inflammation; inflammatory markers; mild cognitive impairmentlcsh:RC321-57103 medical and health sciencesmild cognitive impairment0302 clinical medicineInternal medicinemedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal Researchbusiness.industryNeurodegenerationinflammatory markersmedicine.disease030104 developmental biologyEndocrinologymedicine.anatomical_structureinflammationAgeingmedicine.symptombusinessAlzheimer’s disease030217 neurology & neurosurgeryNeuroscienceFrontiers in Aging Neuroscience
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Biological and biophysics aspects of metformin-induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre-fibrillar aggrega…

2016

The onset of Alzheimer disease (AD) is influenced by several risk factors comprising diabetes. Within this context, antidiabetic drugs, including metformin, are investigated for their effect on AD. We report that in the C57B6/J mice, metformin is delivered to the brain where activates AMP-activated kinase (AMPK), its molecular target. This drug affects the levels of β- secretase (BACE1) and β-amyloid precursor protein (APP), promoting processing and aggregation of β-amyloid (Aβ), mainly in the cortex region. Moreover, metformin induces mitochondrial dysfunction and cell death by affecting the level and conformation of Translocase of the Outer Membrane 40 (TOM40), voltage-dependent anion-sel…

0301 basic medicineAgingmedicine.medical_specialtyMitochondrial poreAmyloidTranslocase of the outer membraneContext (language use)AMP-Activated Protein KinasesBiologyAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineβ-amyloid aggregationAlzheimer DiseaseHexokinaseInternal medicine?-amyloid aggregationmitochondrial dysfunctionmedicineAnimalsHypoglycemic Agentsmitochondrial poresMitochondrial transportAmyloid beta-PeptidesVoltage-Dependent Anion Channel 1BrainAMPKcell degenerationCell BiologyAlzheimer's diseasemedicine.diseaseMitochondriaMetformin030104 developmental biologyEndocrinologyAmyloid Precursor Protein SecretasesAlzheimer's diseasemetforminVDAC1030217 neurology & neurosurgeryResearch Papermedicine.drug
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Hsp60, amateur chaperone in amyloid-beta fibrillogenesis

2016

BACKGROUND: Molecular chaperones are a very special class of proteins that play essential roles in many cellular processes like folding, targeting and transport of proteins. Moreover, recent evidence indicates that chaperones can act as potentially strong suppressor agents in Alzheimer's disease (AD). Indeed, in vitro experiments demonstrate that several chaperones are able to significantly slow down or suppress aggregation of Aβ peptide and in vivo studies reveal that treatment with specific chaperones or their overexpression can ameliorate some distinct pathological signs characterizing AD. METHODS: Here we investigate using a biophysical approach (fluorescence, circular dichroism (CD), t…

0301 basic medicineAmyloidMolecular chaperonesAmyloid betaBiophysicsPlasma protein bindingInhibition mechanismsBiochemistryChaperoninChaperonin03 medical and health sciences0302 clinical medicinemedicineHumansInhibition mechanismMolecular BiologyAmyloid aggregationAmyloid beta-PeptidesbiologyNeurodegenerationP3 peptideFibrillogenesisChaperonin 60medicine.diseaseAlzheimer's disease treatmentCell biology030104 developmental biologyChaperone (protein)biology.proteinHSP60030217 neurology & neurosurgeryProtein BindingBiochimica et Biophysica Acta (BBA) - General Subjects
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Cytoprotective and antioxidant properties of organic selenides for the myelin-forming cells, oligodendrocytes.

2018

Abstract Here a new series of twenty-one organoselenides, of potential protective activity, were synthesized and tested for their intrinsic cytotoxicity, anti-apoptotic and antioxidant capacities in oligodendrocytes. Most of the organoselenides were able to decrease the ROS levels, revealing antioxidant properties. Compounds 5b and 7b showed a high glutathione peroxidase (GPx)-like activities, which were 1.5 folds more active than ebselen. Remarkably, compound 5a diminished the formation of the oligodendrocytes SubG1 peak in a concentration-dependent manner, indicating its anti-apoptotic properties. Furthermore, based on the SwissADME web interface, we performed an in-silico structure-activ…

0301 basic medicineAntioxidantCell Survivalmedicine.medical_treatmentMolecular ConformationApoptosisCrystallography X-RayProtective Agents01 natural sciencesBiochemistryAntioxidantsCell Line03 medical and health scienceschemistry.chemical_compoundMyelinMiceStructure-Activity RelationshipOrganoselenium CompoundsDrug DiscoverymedicineAnimalsCytotoxicityMolecular Biologychemistry.chemical_classification010405 organic chemistryEbselenGlutathione peroxidaseOrganic ChemistryNeurodegenerationCells oligodendrocytesmedicine.diseaseG1 Phase Cell Cycle Checkpoints0104 chemical sciencesOligodendroglia030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryApoptosisDrug DesignReactive Oxygen SpeciesBioorganic chemistry
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Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

2019

The positive role of nutrition in chronic neurodegenerative diseases (NDs) suggests that dietary interventions represent helpful tools for preventing NDs. In particular, diets enriched with natural compounds have become an increasingly attractive, non-invasive, and inexpensive option to support a healthy brain and to potentially treat NDs. Bioactive compounds found in vegetables or microalgae possess special properties able to counteract oxidative stress, which is involved as a triggering factor in neurodegeneration. Here, we briefly review the relevant experimental data on curcuminoids, silymarin, chlorogenic acid, and compounds derived from the microalga Aphanizomenon flos aquae (AFA) whi…

0301 basic medicineAntioxidantsilymarincurcuminoidsPhysiologymedicine.medical_treatmentchlorogenic acidClinical BiochemistryAphanizomenon flos-aquae (dietary supplement)ReviewDiseasePharmacologymedicine.disease_causeBiochemistrySettore BIO/09 - Fisiologia03 medical and health sciencesDietary interventions0302 clinical medicineneurodegenerative diseasemedicineneurodegenerative diseasesMolecular BiologyBeneficial effectsbusiness.industrymicroalgaeNeurodegenerationCell Biologymedicine.disease030104 developmental biologyAphanizomenon flos aquaecurcuminoidbusinessAlzheimer’s disease030217 neurology & neurosurgeryOxidative stress
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