Search results for "NEURODEGENERATIVE DISEASES"

showing 10 items of 155 documents

MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.

2018

The MID1 ubiquitin ligase activates mTOR signaling and regulates mRNA translation. Misregulation of MID1 expression is associated with various diseases including midline malformation syndromes, cancer and neurodegenerative diseases. While this indicates that MID1 expression must be tightly regulated to prevent disease states specific mechanisms involved have not been identified. We examined miRNAs to determine mechanisms that regulate MID1 expression. MicroRNAs (miRNA) are small non-coding RNAs that recognize specific sequences in their target mRNAs. Upon binding, miRNAs typically downregulate expression of these targets. Here, we identified four miRNAs, miR-19, miR-340, miR-374 and miR-542…

0301 basic medicineUntranslated regionSmall interfering RNAPhysiologymetabolism [Microtubule Proteins]Alzheimer's DiseaseBiochemistryImmune PhysiologyMedicine and Health SciencesSmall interfering RNAsmetabolism [Transcription Factors]3' Untranslated RegionsImmune System ProteinsMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionMessenger RNAQRNuclear ProteinsNeurodegenerative DiseasesTranslation (biology)EnzymesUbiquitin ligaseCell biologyNucleic acidsNeurologyMicrotubule ProteinsMedicineOxidoreductasesLuciferasemetabolism [Nuclear Proteins]Research ArticleScienceUbiquitin-Protein LigasesImmunologyTransfectionResearch and Analysis MethodsReal-Time Polymerase Chain ReactionAntibodies03 medical and health sciencesMental Health and PsychiatrymicroRNAGeneticsHumansddc:610Non-coding RNAMolecular Biology TechniquesMolecular BiologyMessenger RNABiology and life sciencesThree prime untranslated regionHEK 293 cellsProteinsGene regulationphysiology [MicroRNAs]MicroRNAs030104 developmental biologyHEK293 CellsEnzymologybiology.proteinRNAProtein TranslationDementiaGene expressionTranscription FactorsMid1 protein human
researchProduct

7-ketocholesterol and 7β-hydroxycholesterol: in vitro and animal models used to characterize their activities and to identify molecules preventing th…

2020

International audience; Oxysterols are molecules derived by the oxidation of cholesterol and can be formed either by auto-oxidation, enzymatically or by both processes. Among the oxysterols formed by auto-oxidation, 7-ketocholesterol and 7beta-hydroxycholesterol are the main forms generated. These oxysterols, formed endogenously and brought in large quantities by certain foods, have major cytotoxic properties. They are powerful inducers of oxidative stress, inducing dysfunction of organelles (mitochondria, lysosomes and peroxisomes) that can cause cell death. These molecules are often identified in increased amounts in common pathological states such as cardiovascular diseases, certain eye …

0301 basic medicine[SDV]Life Sciences [q-bio]CellmicrofluidicMitochondrionPharmacologiemedicine.disease_causeBiochemistry0302 clinical medicineanimal modèleKetocholesterolsComputingMilieux_MISCELLANEOUSCells CulturedsignalingpathwaysCell DeathChemistry7β-hydroxycholesterolNeurodegenerative DiseasesPeroxisomeanimal models3. Good healthmedicine.anatomical_structureBiochemistryCardiovascular Diseases030220 oncology & carcinogenesisToxicity[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]modèle cellulaireSignal transductionProgrammed cell deathCataractCell Line03 medical and health sciencesPharmaceutical sciencesCell Line TumormedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologyhydroxycholestérol7-ketocholesterolPharmacologyOrganelles7-ketocholesterol;7β-hydroxycholesterol;cell models;animal models;microfluidic;signalingpathwaysInflammatory Bowel DiseasesIn vitroHydroxycholesterolscell modelsDisease Models Animal030104 developmental biologyvoie de signalisationSciences pharmaceutiques[SDV.AEN]Life Sciences [q-bio]/Food and NutritionOxidative stress
researchProduct

Antioxidant Alternatives in the Treatment of Amyotrophic Lateral Sclerosis: A Comprehensive Review

2020

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that produces a selective loss of the motor neurons of the spinal cord, brain stem and motor cortex. Oxidative stress (OS) associated with mitochondrial dysfunction and the deterioration of the electron transport chain has been shown to be a factor that contributes to neurodegeneration and plays a potential role in the pathogenesis of ALS. The regions of the central nervous system affected have high levels of reactive oxygen species (ROS) and reduced antioxidant defences. Scientific studies propose treatment with antioxidants to combat the characteristic OS and the regeneration of nicotinamide adenine dinucleotide (NAD+) lev…

0301 basic medicineamyotrophic lateral sclerosispterostilbenePterostilbenePhysiologyCentral nervous systemReviewPharmacologyNicotinamide adenine dinucleotidemedicine.disease_causelcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)mitochondrial dysfunctionmedicineoxidative stressneurodegenerative diseasesAmyotrophic lateral sclerosisnicotinamide ribosidelcsh:QP1-981business.industryNeurodegenerationmedicine.disease030104 developmental biologymedicine.anatomical_structurechemistryNicotinamide ribosideNAD+ kinasebusiness030217 neurology & neurosurgeryOxidative stressFrontiers in Physiology
researchProduct

Physical Activity and Brain Health.

2019

Physical activity (PA) has been central in the life of our species for most of its history, and thus shaped our physiology during evolution. However, only recently the health consequences of a sedentary lifestyle, and of highly energetic diets, are becoming clear. It has been also acknowledged that lifestyle and diet can induce epigenetic modifications which modify chromatin structure and gene expression, thus causing even heritable metabolic outcomes. Many studies have shown that PA can reverse at least some of the unwanted effects of sedentary lifestyle, and can also contribute in delaying brain aging and degenerative pathologies such as Alzheimer’s Disease, diabetes, and multiple s…

0301 basic medicinebrain healthIrisinlcsh:QH426-470Dopaminemyokinesphysical activityDiseaseReviewmyokineexercise and neurodegenerationexercise and aging03 medical and health sciences0302 clinical medicineSettore BIO/10 - BiochimicaMyokineGeneticsMedicineHumansEpigeneticsSettore BIO/06 - Anatomia Comparata E CitologiaExerciseGenetics (clinical)Sedentary lifestylelactatebusiness.industryMultiple sclerosisBrain-Derived Neurotrophic FactorBrainCognitionNeurodegenerative Diseasesmedicine.diseaselcsh:Genetics030104 developmental biologyBDNFAntidepressantbusinessNeuroscience030217 neurology & neurosurgeryHormoneEndocannabinoidsGenes
researchProduct

Studying the blood-brain barrier will provide new insights into neurodegeneration - Commentary.

2018

0301 basic medicinebusiness.industryMultiple sclerosisNeurodegenerationNeurodegenerative DiseasesBlood–brain barriermedicine.disease03 medical and health sciences030104 developmental biologymedicine.anatomical_structureNeurologyBlood-Brain BarriermedicineAnimalsHumansNeurology (clinical)businessNeuroscienceMultiple sclerosis (Houndmills, Basingstoke, England)
researchProduct

Vitamin D and the nervous system

2019

Objective: to summarise the activities that Vitamin D (VD) carries out in the brain and to clarify the potential role of VD in neurological diseases. Methods: a literature research has been performed in Pubmed using the following keywords: 'Vitamin D', 'nervous system', 'brain'. Results: the studies reviewed show that VD contributes to cerebral activity in both embryonic and adult brain, helping the connectivity of neural circuits responsible for locomotor, emotional and reward-dependent behavior. Low VD serum levels have been found in patients affected by Alzheimer Disease, Parkinson Disease, Multiple Sclerosis, Autism Spectrum Disorders, Sleep Disorders and Schizophrenia. Discussion: find…

0301 basic medicinecognitionMultiple SclerosisbrainDiseaseBioinformaticsCalcitriol receptorNervous Systemvitamin D deficiency03 medical and health sciences0302 clinical medicineMultiple SclerosimedicineVitamin D and neurologyHumansVitamin DVDRNeurodegenerative Diseasebusiness.industryMultiple sclerosisNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseVitamin D Deficiencybehaviour030104 developmental biologyNeurologySchizophreniaAutismReceptors CalcitriolNeurology (clinical)Alzheimer's diseasebusiness030217 neurology & neurosurgeryHuman
researchProduct

Neurological aspects of medical use of cannabidiol

2017

Background: Cannabidiol (CBD) is among the major secondary metabolites of Cannabis devoid of the delta-9-tetra-hydrocannabinol psychoactive effects. It is a resorcinol-based compound with a broad spectrum of potential therapeutic properties, including neuroprotective effects in numerous pathological conditions. CBD neuroprotection is due to its antioxidant and antiinflammatory activities and the modulation of a large number of brain biological targets (receptors, channels) involved in the development and maintenance of neurodegenerative diseases. Objective: The aim of the present review was to describe the state of art about the pre-clinical research, the potential use and, when existing, t…

0301 basic medicinemedicine.medical_specialtyNeurologyCannabidiol; Neurodegenerative diseases; Neurological; Neurology; Neuroprotection; Neuroscience (all); PharmacologyDiseaseBioinformaticsNeurodegenerative diseaseNeuroprotection03 medical and health sciences0302 clinical medicineSettore MED/43 - Medicina LegaleCentral Nervous System DiseasesMedicineAnimalsCannabidiolHumansneurodegenerative diseasesYoung adultAmyotrophic lateral sclerosisPharmacologyNeuroscience (all)biologybusiness.industryGeneral NeuroscienceMultiple sclerosismedicine.diseasebiology.organism_classificationNeuroprotection030104 developmental biologyNeuroprotective AgentsNeurologyNeurologicalcannabidiol; neurodegenerative diseases; neurological; neurology; neuroprotectionCannabisbusinessCannabidiol030217 neurology & neurosurgerymedicine.drug
researchProduct

Role of p27Kip1 as a transcriptional regulator

2018

The protein p27Kip1 is a member of the Cip/Kip family of cyclin-dependent kinase (Cdk) inhibitors. It interacts with both the catalytic and the regulatory subunit (cyclin) and introduces a region into the catalytic cleave of the Cdk inducing its inactivation. Its inhibitory capacity can be modulated by specific tyrosine phosphorylations. p27Kip1 also behaves as a transcriptional regulator. It associates with specific chromatin domains through different transcription factors. ChIP on chip, ChIP-seq and expression microarray analysis allowed the identification of the transcriptional programs regulated by p27Kip1. Thus, important cellular functions as cell division cycle, respiration, RNA proc…

0301 basic medicinep27Kip1Review03 medical and health sciencesTranscriptional regulationCyclin-dependent kinaseTranscription (biology)Gene expressionTranscriptional regulationcancertranscriptional regulationNeurodegenerationCàncerTranscription factorE2F4CancerbiologyChemistryMalalties neurodegenerativesneurodegenerationNeurodegenerative DiseasesChIP-on-chipExpressió gènicaCell biologyChromatin030104 developmental biologyOncologybiology.proteinGene expressionOncotarget
researchProduct

Tryptophan-Containing Dual Neuroprotective Peptides: Prolyl Endopeptidase Inhibition and Caenorhabditis elegans Protection from β-Amyloid Peptide Tox…

2018

Neuroprotective peptides represent an attractive pharmacological strategy for the prevention or treatment of age-related diseases, for which there are currently few effective therapies. Lactoferrin (LF)-derived peptides (PKHs) and a set of six rationally-designed tryptophan (W)-containing heptapeptides (PACEIs) were characterized as prolyl endopeptidase (PEP) inhibitors, and their effect on β-amyloid peptide (Aβ) toxicity in a Caenorhabditis elegans model of Alzheimer’s disease (AD) was evaluated. Two LF-derived sequences, PKH8 and PKH11, sharing a W at the C-terminal end, and the six PACEI heptapeptides (PACEI48L to PACEI53L) exhibited significant in vitro PEP inhibition. The inhibitory pe…

0301 basic medicineprolyl endopeptidase inhibitionPeptidelactoferrin-derived peptidesPharmacologyNeuroprotectionCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciencesneurodegenerative diseases; amyloid β peptide; <i>Caenorhabditis elegans</i>; prolyl endopeptidase inhibition; lactoferrin-derived peptides; rationally-designed peptides; tryptophan; molecular docking0302 clinical medicineProlyl endopeptidaseIn vivomedicineneurodegenerative diseasestryptophanPhysical and Theoretical ChemistryCaenorhabditis eleganslcsh:QH301-705.5Molecular BiologySpectroscopyCaenorhabditis elegansamyloid β peptidechemistry.chemical_classificationbiologyOrganic ChemistryTryptophanmolecular dockingGeneral Medicinebiology.organism_classificationIn vitroComputer Science Applications030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryrationally-designed peptidesToxicity030217 neurology & neurosurgerymedicine.drugInternational Journal of Molecular Sciences; Volume 19; Issue 5; Pages: 1491
researchProduct

The Role of Adrenoceptors in the Retina

2020

The retina is a part of the central nervous system, a thin multilayer with neuronal lamination, responsible for detecting, preprocessing, and sending visual information to the brain. Many retinal diseases are characterized by hemodynamic perturbations and neurodegeneration leading to vision loss and reduced quality of life. Since catecholamines and respective bindings sites have been characterized in the retina, we systematically reviewed the literature with regard to retinal expression, distribution and function of alpha1 (α1)-, alpha2 (α2)-, and beta (β)-adrenoceptors (ARs). Moreover, we discuss the role of the individual adrenoceptors as targets for the treatment of retinal diseases.

0301 basic medicineretinaAdrenergic receptorgenetic structuresCentral nervous systemReviewα<sub>1</sub>-ARBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRetinal DiseasesmedicinedistributionAnimalsHumansα1-ARlcsh:QH301-705.5NeuronsRetinafunctionBinding Sitesα<sub>2</sub>-ARNeurodegenerationRetinalNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseeye diseasesReceptors Adrenergic030104 developmental biologymedicine.anatomical_structurechemistrylcsh:Biology (General)β-ARNeuroscience030217 neurology & neurosurgeryα2-ARCells
researchProduct