Search results for "Neurodegenerative Disease"

showing 10 items of 169 documents

Vascular ageing and the related complications in the brain: New insights on related mechanisms and their translational applications

2021

s consequence of “populations aging phenomenon”, the burden of incessant increase of incidence and prevalence of neurodegenerative diseases (NeuroDegD) is becoming very alarming, as well as it is gaining an important attention the developing of intervention measures, essen-tially preventive. Of consequence, the knowledge of primordial Neuro-DegD causes, and the related mechanisms, appears to be fundamental. Consistent with this, growing evidence reports a close link of the vascular aging, dysfunction and diseases with the onset and progression of NeuroDegD.

Agingbusiness.industryMEDLINEBrainNeurodegenerative DiseasesBioinformaticsCardiovascular SystemVascular ageingCerebrovascular DisordersText miningCognitive AgingSettore MED/05 - Patologia ClinicaHumansMedicineVascular ageing and the related complicationbusinessneurodegenerative diseases (NeuroDegD)Developmental BiologyMechanisms of Ageing and Development
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Antioxidants as a Potential Therapy Against Age-Related Neurodegenerative Diseases: Amyloid Beta Toxicity and Alzheimers Disease

2006

Alzheimer's disease (AD) is a progressive age-related neurodegenerative disorder with distinct neuropathological features. Extracellular plaques, consisting of aggregated amyloid peptides of 39-43 amino acids are one of the most prominent pathological hallmarks of this disease. Although the exact neurochemical effector mechanism of Abeta aggregation is not yet elucidated, age-associated disturbances of metal ion metabolism have been proposed to promote the formation of aggregates from soluble Abeta. Oxidative stress is postulated to be a downstream effect of Abeta-metal ion interactions. Therefore, the modulation of brain metal metabolism and attenuation of oxidative stress by antioxidant m…

Agingmedicine.medical_specialtyAntioxidantAmyloidAmyloid betamedicine.medical_treatmentPharmacologymedicine.disease_causeAntioxidantsNeurochemicalDegenerative diseaseAlzheimer DiseaseInternal medicinemental disordersDrug DiscoverymedicineAnimalsHumansPharmacologyAmyloid beta-PeptidesMetal metabolismbiologyChemistryNeurodegenerative Diseasesmedicine.diseaseEndocrinologybiology.proteinAlzheimer's diseaseOxidative stressCurrent Pharmaceutical Design
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The emerging role of miRNA-132/212 cluster in neurologic and cardiovascular diseases: Neuroprotective role in cells with prolonged longevity

2021

Abstract miRNA-132/212 are small regulators of gene expression with a function that fulfills a vital function in diverse biological processes including neuroprotection of cells with prolonged longevity in neurons and the cardiovascular system. In neurons, miRNA-132 appears to be essential for controlling differentiation, development, and neural functioning. Indeed, it also universally promotes axon evolution, nervous migration, plasticity as well, it is suggested to be neuroprotective against neurodegenerative diseases. Moreover, miRNA-132/212 disorder leads to neural developmental perturbation, and the development of degenerative disorders covering Alzheimer’s, Parkinson’s, and epilepsy’s …

Agingmedicine.medical_specialtyNeurologyDegenerative Disordermedia_common.quotation_subjectNeuroprotection03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansMedicineMyocytes CardiacMolecular Targeted TherapyAxonCellular SenescenceComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonNeurons0303 health sciencesbusiness.industryNeurodegenerationAutophagyLongevityNeurodegenerative Diseasesmedicine.diseaseNeuroprotection3. Good healthMicroRNAsmedicine.anatomical_structureGene Expression RegulationCardiovascular DiseasesbusinessNeuroscience030217 neurology & neurosurgeryDevelopmental Biology
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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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Emerging contributions of formyl peptide receptors to neurodegenerative diseases.

2021

Abstract Inflammation is a central element of many neurodegenerative diseases. Formyl peptide receptors (FPRs) can trigger several receptor-dependent signal transduction pathways that play a key role in neuroinflammation and neurodegeneration. They are chemotactic receptors that help to regulate pro- and anti-inflammatory responses in most mammals. FPRs are primarily expressed in the immune and nervous systems where they interact with a complex pattern of pathogen-derived and host-endogenous molecules. Mounting evidence points towards a contribution of FPRs – via neuropathological ligands such as Amyloid beta, and neuroprotective ligands such as Humanin, Lipoxin A4, and Annexin A1 – to mult…

Amyloid beta-PeptidesClinical BiochemistryNeurodegenerationChemotaxisNeurodegenerative DiseasesBiologymedicine.diseaseLigandsBiochemistryNeuroprotectionReceptors Formyl PeptideNeuroinflammatory DiseasesmedicineFunctional selectivityAnimalsHumansSignal transductionMolecular BiologyCentral elementNeuroscienceNeuroinflammationHumaninBiological chemistryReferences
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The neuroprotective potential of carotenoids in vitro and in vivo.

2021

Abstract Background Despite advances in research on neurodegenerative diseases, the pathogenesis and treatment response of neurodegenerative diseases remain unclear. Recent studies revealed a significant role of carotenoids to treat neurodegenerative diseases. The aim of this study was to systematically review the neuroprotective potential of carotenoids in vivo and in vitro and the molecular mechanisms and pathological factors contributing to major neurodegenerative diseases (Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, and stroke). Hypothesis Carotenoids as therapeutic molecules to target neurodegenerative diseases. Results Aggregation of …

Antioxidantmedicine.medical_treatmentCrocetinPharmaceutical ScienceDiseasePharmacologymedicine.disease_causeNeuroprotectionAntioxidantschemistry.chemical_compoundIn vivoDrug DiscoverymedicineHumansCarotenoidNeuroinflammationPharmacologychemistry.chemical_classificationbusiness.industryNeurodegenerative DiseasesCarotenoidsNeuroprotectionOxidative StressNeuroprotective AgentsComplementary and alternative medicinechemistryMolecular MedicinebusinessOxidative stressPhytomedicine : international journal of phytotherapy and phytopharmacology
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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Hsp70 and Its Molecular Role in Nervous System Diseases

2011

Heat shock proteins (HSPs) are induced in response to many injuries including stroke, neurodegenerative disease, epilepsy, and trauma. The overexpression of one HSP in particular, Hsp70, serves a protective role in several different models of nervous system injury, but has also been linked to a deleterious role in some diseases. Hsp70 functions as a chaperone and protects neurons from protein aggregation and toxicity (Parkinson disease, Alzheimer disease, polyglutamine diseases, and amyotrophic lateral sclerosis), protects cells from apoptosis (Parkinson disease), is a stress marker (temporal lobe epilepsy), protects cells from inflammation (cerebral ischemic injury), has an adjuvant role i…

Autoimmune diseasebusiness.industryMultiple sclerosisNeurodegenerationReview ArticleDiseaseHsp70 nervous system neurodegenerative diseasesmedicine.diseaseBiochemistrylcsh:BiochemistryCellular stress responseHeat shock proteinImmunologymedicinelcsh:QD415-436Alzheimer's diseaseAmyotrophic lateral sclerosisbusinessBiochemistry Research International
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p62: Friend or Foe? Evidences for OncoJanus and NeuroJanus Roles

2020

p62 is a versatile protein involved in the delicate balance between cell death and survival, which is fundamental for cell fate decision in the context of both cancer and neurodegenerative diseases. As an autophagy adaptor, p62 recognizes polyubiquitin chains and interacts with LC3, thereby targeting the selected cargo to the autophagosome with consequent autophagic degradation. Beside this function, p62 behaves as an interactive hub in multiple signalling including those mediated by Nrf2, NF-κB, caspase-8, and mTORC1. The protein is thus crucial for the control of oxidative stress, inflammation and cell survival, apoptosis, and metabolic reprogramming, respectively. As a multifunctional pr…

AutophagosomeProgrammed cell deathP62ApoptosisContext (language use)mTORC1Cell fate determinationBiologyCatalysislcsh:ChemistryInorganic ChemistryStress granuleAutophagymedicinePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCancerNeurodegenerative diseasesOrganic ChemistryNeurodegenerationAutophagyGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologylcsh:Biology (General)lcsh:QD1-999International Journal of Molecular Sciences
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A Neuroprotective Function for the Hematopoietic Protein Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF)

2007

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine responsible for the proliferation, differentiation, and maturation of cells of the myeloid lineage, which was cloned more than 20 years ago. Here we uncovered a novel function of GM-CSF in the central nervous system (CNS). We identified the GM-CSF α-receptor as an upregulated gene in a screen for ischemia-induced genes in the cortex. This receptor is broadly expressed on neurons throughout the brain together with its ligand and induced by ischemic insults. In primary cortical neurons and human neuroblastoma cells, GM-CSF counteracts programmed cell death and induces BCL-2 and BCL-Xl expression in a dose- a…

Brain InfarctionMaleProgrammed cell deathTime FactorsMyeloidmedicine.medical_treatmentDrug Evaluation Preclinicalbcl-X ProteinApoptosisBiologyNeuroprotectionBrain IschemiaPhosphatidylinositol 3-KinasesmedicineAnimalsHumansMyeloid CellsRats Long-EvansRats WistarProtein kinase BCell ProliferationCerebral CortexNeuronsDose-Response Relationship DrugGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationNeurodegenerative DiseasesRatsUp-RegulationCell biologyDisease Models AnimalHaematopoiesisNeuroprotective Agentsmedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorNeurologyBlood-Brain BarrierReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologyNeurology (clinical)Signal transductionCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktSignal Transductionmedicine.drugJournal of Cerebral Blood Flow & Metabolism
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