Search results for "NeuroD"

showing 10 items of 604 documents

Heat shock protein (Hsp) regulation by muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus.

2018

The cholinergic system plays a crucial role in modulating in the central nervous system physiological responses such as neurogenesis, neuronal differentiation, synaptic plasticity, and neuroprotection. In a recent study, we showed that Oxotremorine-M, a non-selective muscarinic acetylcholine receptor agonist, is able to transactivate the fibroblast growth factor receptor and to produce a significant increase in the hippocampal primary neurite outgrowth. In the present study we aimed to explore in the rat hippocampus the possible effect of acute or chronic treatment with Oxotremorine-M on some heat shock proteins (Hsp60, Hsp70, Hsp90) and on activation of related transcription factor heat sh…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPhysiologyClinical BiochemistryNeuronal OutgrowthScopolamineheat shock proteinHsp90NeuroprotectionHippocampusHsp7003 medical and health sciencesmuscarinic receptor0302 clinical medicineHeat Shock Transcription FactorsHeat shock proteinInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineAnimalsRats WistarHSF1Heat-Shock ProteinsNeuronsNeuronal PlasticityChemistryOxotremorineNeurodegenerative DiseasesCell BiologyReceptors Fibroblast Growth FactorReceptors MuscarinicHsp70Rats030104 developmental biologyEndocrinologyheat shock factor 1HSP60030217 neurology & neurosurgerymedicine.drugSignal TransductionJournal of cellular physiology
researchProduct

Curcumin-like compounds designed to modify amyloid beta peptide aggregation patterns

2017

International audience; Curcumin is a natural polyphenol able to bind the amyloid beta peptide, which is related to Alzheimer's disease, and modify its self-assembly pathway. This paper focuses on a multi-disciplinary study that starts from the design of curcumin-like compounds with the key chemical features required for inhibiting amyloid beta aggregation, and reports the effects of these compounds on the in vitro aggregation of amyloid beta peptides. Chemoinformatic screening was performed through the calculation of molecular descriptors that were able to highlight the drug-like profile, followed by docking studies with an amyloid beta peptide fibril. The computational design underlined t…

0301 basic medicineAmyloid betaGeneral Chemical Engineering[SDV]Life Sciences [q-bio]PeptideFibrillaw.inventionChemical compounds03 medical and health scienceschemistry.chemical_compoundConfocal microscopylawMolecular descriptorDiagnosisFluorescence spectroscopyGlycoproteinschemistry.chemical_classificationbiologyNeurodegenerative diseasesProteinsAlzheimer amyloid peptide oxadiazole curcuminGeneral ChemistrySettore CHIM/06 - Chimica OrganicaIn vitro030104 developmental biologychemistryBiochemistryDocking (molecular)Curcuminbiology.proteinCell culturePeptides
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Epilepsy in neuropathologically verified Alzheimer's disease.

2018

Abstract Purpose Subjects with Alzheimer's disease (AD) have been shown to be at a higher risk for epilepsy. The vast majority of the previous studies have not included a full neuropathological examination. Methods The objective of this study was to assess the prevalence of epilepsy and clinicopathological characteristics in a well-defined study group of 64 subjects with AD. We evaluated the clinicopathological findings in 64 subjects (mean age at death 85 ± 8.6 years) from a longitudi-nal study cohort of patients with dementia. Results Eleven out of the 64 subjects (17%) had a history of epilepsy, which is comparable to previous studies. The subjects with AD and epilepsy were significantly…

0301 basic medicineApolipoprotein EMalemedicine.medical_specialtyNeurologyTime FactorsalzheimerAutopsyNeuropathologyDiseaseAlzheimerin tauti03 medical and health sciencesEpilepsyautopsy0302 clinical medicineApolipoproteins EAlzheimer DiseaseInternal medicinemedicinePrevalenceDementiaHumansneurodegenerative diseasesLongitudinal Studiesta515ta316Aged 80 and overEpilepsybusiness.industryneurodegenerationAge FactorsBrainGeneral MedicineAlzheimer's diseasemedicine.diseaseneurodegeneratiiviset sairaudetHospitalization030104 developmental biologyNeurologyruumiinavausCohortFemaleNeurology (clinical)businessepilepsia030217 neurology & neurosurgerydementiaFollow-Up StudiesSeizure
researchProduct

PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia

2020

Friedreich ataxia (FRDA), the most common autosomal recessive ataxia, is characterized by degeneration of the large sensory neurons and spinocerebellar tracts, cardiomyopathy, and increased incidence in diabetes. The underlying pathophysiological mechanism of FRDA, driven by a significantly decreased expression of frataxin (FXN), involves increased oxidative stress, reduced activity of enzymes containing iron‑sulfur clus-ters (ISC), defective energy production, calcium dyshomeostasis, and impaired mitochondrial biogenesis, leading to mitochondrial dysfunction. The peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcriptional factor playing a key role in mito…

0301 basic medicineAtaxiaCell SurvivalCaspase 3PPAR agonistlcsh:RC321-57103 medical and health sciencesMice0302 clinical medicineIron-Binding ProteinsmedicineNeuritesAnimalsHumansMyocytes CardiacNeurodegenerationDorsal root ganglia neuronslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMembrane Potential MitochondrialNeuronsCardiomyocytesbiologyChemistryFrataxinNeurodegenerationCalpainLipid DropletsPeroxisomemedicine.diseaseCell biologyMitochondriaRatsPPAR gamma030104 developmental biologyNeurologyMitochondrial biogenesisFriedreich AtaxiaFrataxinbiology.proteinThiazolidinedionesmedicine.symptomMitochondrial function030217 neurology & neurosurgery
researchProduct

Reversible Axonal Dystrophy by Calcium Modulation in Frataxin-Deficient Sensory Neurons of YG8R Mice

2017

15 Pages, 8 Figures. The Supplementary Material for this article can be found online at: http://journal.frontiersin.org/article/10.3389/fnmol.2017.00264/full#supplementary-material

0301 basic medicineAtaxiaNeuriteFriedreich’s ataxiarare diseaseMitochondrionlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBAPTAmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyOriginal ResearchcalciumbiologyNeurodegenerationneurodegenerationFriedreich's ataxiaaxonal spheroidsmedicine.disease3. Good healthmitochondria030104 developmental biologyPeripheral neuropathychemistrynervous systemFrataxinbiology.proteinAxoplasmic transportmedicine.symptomNeuroscience030217 neurology & neurosurgeryNeuroscience
researchProduct

Oxidative Stress, a Crossroad Between Rare Diseases and Neurodegeneration

2020

Oxidative stress is an imbalance between production and accumulation of oxygen reactive species and/or reactive nitrogen species in cells and tissues, and the capacity of detoxifying these products, using enzymatic and non-enzymatic components, such as glutathione. Oxidative stress plays roles in several pathological processes in the nervous system, such as neurotoxicity, neuroinflammation, ischemic stroke, and neurodegeneration. The concepts of oxidative stress and rare diseases were formulated in the eighties, and since then, the link between them has not stopped growing. The present review aims to expand knowledge in the pathological processes associated with oxidative stress underlying …

0301 basic medicineAtaxiaUnverricht–Lundborg disease (ULD)PhysiologyNeurodegeneration with brain iron accumulationClinical BiochemistryFriedreich’s ataxiaReviewmedicine.disease_causeBioinformaticsBiochemistry03 medical and health scienceschemistry.chemical_compoundLafora disease (LD)0302 clinical medicineMedicineprogressive myoclonus epilepsy (PME)Molecular BiologyNeuroinflammationReactive nitrogen speciesneurodegenerative disorders with brain iron accumulation (NBIA)business.industryNeurodegenerationlcsh:RM1-950NeurotoxicityCell Biologymedicine.diseaseDravet syndromeCharcot-Marie-Tooth disease (CMT)030104 developmental biologylcsh:Therapeutics. Pharmacologychemistrymedicine.symptombusinessMyoclonusinherited retinal dystrophy (IRD)030217 neurology & neurosurgeryOxidative stressAntioxidants
researchProduct

DLG4-related synaptopathy: a new rare brain disorder

2021

Contains fulltext : 245031.pdf (Publisher’s version ) (Closed access) PURPOSE: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. METHODS: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. RESULTS: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit-hyp…

0301 basic medicineAutism Spectrum Disorder[SDV]Life Sciences [q-bio]030105 genetics & heredityBiology03 medical and health sciencesIntellectual DisabilityIntellectual disabilitymedicineMissense mutationHumansGlobal developmental delayExomeGenetics (clinical)GeneticsBrain DiseasesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Brainmedicine.disease030104 developmental biologyPhenotypeRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Autism spectrum disorderNeurodevelopmental DisordersSynaptopathyDLG4Postsynaptic densityDisks Large Homolog 4 Protein
researchProduct