Search results for "generation"

showing 10 items of 3050 documents

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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Cellular and molecular basis of the imbalance between vascular damage and repair in ageing and age-related diseases: As biomarkers and targets for ne…

2016

Preclinical and clinical studies suggest that specific subsets of cells isolated from the peripheral blood, play an essential role in the imbalance of damage and repair during age-associated diseases, such as metabolic syndrome, diabetes, atherosclerosis, neurodegenerative diseases, osteoporosis and cancer. Endogenous regeneration of the vessel wall involves cells of the vascular wall, inflammatory cells, circulating precursors, and mature endothelial cells, which are capable to restore the endothelium in a concerted interaction. Early detection of such imbalances with specific biomarkers may reduce age-associated diseases and subsequent cardiovascular events. Likewise, new strategies have …

0301 basic medicineAgingEndotheliumCellStimulationBiologyVascular disease03 medical and health sciencesDiabetes mellitusStem and progenitor cellsNeoplasmsmedicineBiomarkers TumorDiabetes MellitusStem and progenitor cells Biomarkers Ageing Vascular diseaseAnimalsHumansMetabolic SyndromeTumorVascular diseaseEndogenous regenerationCancerNeurodegenerative Diseasesmedicine.diseaseAtherosclerosisAgeing; Biomarkers; Stem and progenitor cells; Vascular disease; Animals; Biomarkers Tumor; Humans; Aging; Atherosclerosis; Diabetes Mellitus; Metabolic Syndrome; Neoplasms; Neurodegenerative Diseases; OsteoporosisAgeing030104 developmental biologymedicine.anatomical_structureAgeingImmunologyCancer researchOsteoporosisBiomarkersDevelopmental Biology
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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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“Pro-youthful” factors in the “labyrinth” of cardiac rejuvenation

2016

IF 3.350; International audience; The mechanisms of aging and senescence include various endogenous and exogenous factors. Among cardiovascular diseases, heart failure is a typical age-related disease. New strategies to restore cardiomyocyte cells have been reported: endogenous substances that can regenerate the heart's cardiomyocytes have been described: follistatin like 1 (FSTL1), growth-differentiation factor 11 (GDF11) and insulin-like growth factor 1 (IGF-I). Manipulation of the different anti and pro-pathways is essential to discover new approaches to regenerative therapies. (C) 2016 Elsevier Inc. All rights reserved.

0301 basic medicineAgingStem-Cellsmedicine.medical_treatmentEndogenyCardiovascular-DiseaseBioinformaticsBiochemistryEndocrinologyFollistatin-Like 1Myocytes CardiacInsulin-Like Growth Factor Ibiology[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyGrowth differentiation factorGrowth-Factor-I3. Good healthIGF-IGrowth Differentiation FactorsBone Morphogenetic ProteinsCardiacMouse HeartSenescencemedicine.medical_specialtyFollistatin-Related ProteinsGene-Expression[ SDV.MHEP.GEG ] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyFSTL1Mammalian Heart03 medical and health sciencesMyocardial-InfarctionInternal medicineGeneticsmedicineHumansRegenerationRejuvenationMolecular BiologyHeart FailureYoung BloodTelomerase ExpressionRegeneration (biology)Growth factorCell Biologymedicine.disease030104 developmental biologyEndocrinologyHeart failureGDF11GDF11biology.proteinFollistatin
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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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5-HT1A Receptor Function Makes Wound Healing a Happier Process

2018

Skin wound healing is a multistage phenomenon that is regulated by cell–cell interplay and various factors. Endogenous serotonin is an important neurotransmitter and cytokine. Its interaction with the serotonin 1A receptor (5-HTR1A) delivers downstream cellular effects. The role of serotonin (5-hydroxytryptamine, 5-HT) and the 5-HT1A receptor has been established in the regeneration of tissues such as the liver and spinal motor neurons, prompting the investigation of the role of 5-HT1A receptor in skin healing. This study assessed the role of 5-HT1A receptor in excisional wound healing by employing an excisional punch biopsy model on 5-Ht1a receptor knockout mice. Post-harvest analysis reve…

0301 basic medicineAgonistmedicine.drug_classmedicine.medical_treatmentwound healingPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineskin regenerationmedicine5-HT1A receptorPharmacology (medical)NeurotransmitterReceptor5-Ht1a receptor knockout mice modelOriginal ResearchPharmacologySkin repairintegumentary systembusiness.industrylcsh:RM1-950serotonin3. Good healthlcsh:Therapeutics. Pharmacology030104 developmental biologyCytokinenervous systemchemistry030220 oncology & carcinogenesisKnockout mouse5-HT1A receptorWound healingbusinessFrontiers in Pharmacology
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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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