Search results for "neurotoxicity"

showing 10 items of 105 documents

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
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Overview of General and Discriminating Markers of Differential Microglia Phenotypes.

2020

Inflammatory processes and microglia activation accompany most of the pathophysiological diseases in the central nervous system. It is proven that glial pathology precedes and even drives the development of multiple neurodegenerative conditions. A growing number of studies point out the importance of microglia in brain development as well as in physiological functioning. These resident brain immune cells are divergent from the peripherally infiltrated macrophages, but their precise in situ discrimination is surprisingly difficult. Microglial heterogeneity in the brain is especially visible in their morphology and cell density in particular brain structures but also in the expression of cell…

0301 basic medicineCentral nervous systemInflammationReviewBiologylcsh:RC321-571M1/M2 phenotype03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineImmune systemneurotoxicitymedicineCytotoxic T celllcsh:Neurosciences. Biological psychiatry. NeuropsychiatrypolarizationMicrogliaRegeneration (biology)Neurotoxicityinfiltrating macrophagesmedicine.diseasePhenotype030104 developmental biologymedicine.anatomical_structureinflammationCellular Neuroscienceregenerationmicroglial heterogeneitymedicine.symptomNeuroscience030217 neurology & neurosurgeryFrontiers in cellular neuroscience
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Enhancement in Phospholipase D Activity as a New Proposed Molecular Mechanism of Haloperidol-Induced Neurotoxicity

2020

Membrane phospholipase D (PLD) is associated with numerous neuronal functions, such as axonal growth, synaptogenesis, formation of secretory vesicles, neurodegeneration, and apoptosis. PLD acts mainly on phosphatidylcholine, from which phosphatidic acid (PA) and choline are formed. In turn, PA is a key element of the PLD-dependent secondary messenger system. Changes in PLD activity are associated with the mechanism of action of olanzapine, an atypical antipsychotic. The aim of the present study was to assess the effect of short-term administration of the first-generation antipsychotic drugs haloperidol, chlorpromazine, and fluphenazine on membrane PLD activity in the rat brain. Animals were…

0301 basic medicineFluphenazineolanzapinePhospholipasePharmacologyCatalysishaloperidollcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineneurotoxicityHaloperidolmedicineAnimalsphospholipase DPhospholipase D activityPhysical and Theoretical ChemistryChlorpromazinechlorpromazinelcsh:QH301-705.5Molecular BiologySpectroscopy030102 biochemistry & molecular biologyPhospholipase DCommunicationOrganic ChemistryGeneral MedicinePhosphatidic acidfluphenazineRatsComputer Science ApplicationsEnzyme Activationenzymes and coenzymes (carbohydrates)lcsh:Biology (General)lcsh:QD1-999chemistryMechanism of actionneuroprotectionlipids (amino acids peptides and proteins)medicine.symptom030217 neurology & neurosurgerymedicine.drugInternational Journal of Molecular Sciences
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Hg and Se exposure in brain tissues of striped dolphin (Stenella coeruleoalba) and bottlenose dolphin (Tursiops truncatus) from the Tyrrhenian and Ad…

2017

In this study we analyzed Hg and Se concentrations in dolphin brain tissues of fifteen specimens of striped dolphin (Stenella coeruleoalba) and eight specimens of bottlenose dolphin (Tursiops truncatus) stranded in the Tyrrhenian and Adriatic Seas, in order to assess the toxicological risks associated with Hg exposure. High Hg concentrations were found in brain tissues of both analyzed specie (1.86–243 mg/kg dw for striped dolphin and 2.1–98.7 mg/kg dw for bottlenose dolphin), exceeding levels associated with marine mammals neurotoxicity. Althougth the results clearly suggest that the protective effects of Se against Hg toxicity occur in cetaceans’ brain tissues, a molar excess of mercury w…

0301 basic medicineHealth Toxicology and MutagenesisZoologyStenella coeruleoalba010501 environmental sciencesBiologyManagement Monitoring Policy and LawToxicology01 natural sciencesAquatic organisms03 medical and health sciencesSeleniumStenellabiology.animalNeurotoxicityAnimalsSettore CHIM/01 - Chimica Analitica0105 earth and related environmental sciencesBrain; Mercury; Neurotoxicity; Selenium; Stenella coeruleoalba; Tursiops truncatus; Animals; Bottle-Nosed Dolphin; Brain; Italy; Mercury; Selenium; Stenella; Water Pollutants; Risk assessmentAnimalBrainAquatic animalGeneral MedicineMercuryBottlenose dolphinbiology.organism_classificationFisheryBottle-Nosed Dolphin030104 developmental biologyItalyStenella coeruleoalbaTursiops truncatuhuman activitiesWater Pollutants ChemicalEcotoxicology (London, England)
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Binding and neurotoxicity mitigation of toxic tau oligomers by synthetic heparin like oligosaccharides.

2018

Well-defined heparin like oligosaccharides up to decasaccharides were synthesized. It was discovered for the first time that heparin oligosaccharides, as short as tetrasaccharides, can bind with the most toxic tau species, i.e., tau oligomers with nM KD. The binding significantly reduced the cellular uptake of toxic tau oligomers and protected the cells from tau oligomer induced cytotoxicity.

0301 basic medicineHeparin likeMetals and AlloysNeurotoxicityGeneral ChemistryHeparinmedicine.diseaseOligomerCatalysisArticleSurfaces Coatings and FilmsElectronic Optical and Magnetic Materials03 medical and health scienceschemistry.chemical_compound030104 developmental biologyBiochemistrychemistrymental disordersMaterials ChemistryCeramics and CompositesmedicineCytotoxicitymedicine.drugChemical communications (Cambridge, England)
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In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity.

2015

In multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)-induced excitotoxicity, leading to toxic increases in intraneuronal Ca(2+) . Here, we used in vivo two-photon imaging in the brain of TN-XXL transgenic Ca(2+) reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod-phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T-helper 17 ly…

0301 basic medicineKainic acidMultiple SclerosisExcitotoxicityGlutamic AcidPharmacologyBiologymedicine.disease_causeBiochemistryNeuroprotectionImmunomodulation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsCells CulturedNeuronsKainic AcidDimethyl fumarateCell DeathGlutamate receptorNeurotoxicityBrainmedicine.diseaseUp-Regulation030104 developmental biologyNeuroprotective AgentschemistryNMDA receptor030217 neurology & neurosurgerySignal TransductionJournal of neurochemistry
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Multicomponent Training Prevents Memory Deficit Related to Amyloid-β Protein-Induced Neurotoxicity.

2021

Background: Alzheimer’s disease (AD) is characterized by the accumulation of the amyloid-β peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. Objective: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aβ neurotoxicity. Methods: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-β peptide into their hippocampus. Results: We show that long-term multicomponent training prevents …

0301 basic medicineMaleHippocampusPhysical exercisePharmacologyHippocampal formationmedicine.disease_causeHippocampusLipid peroxidationStereotaxic Techniques03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysical Conditioning AnimalMedicineAnimalsRats WistarRecognition memoryMemory DisordersAmyloid beta-Peptidesbusiness.industryGeneral NeuroscienceNeurotoxicityBrainGeneral Medicinemedicine.diseaseRatsPsychiatry and Mental healthClinical PsychologyDisease Models AnimalOxidative Stress030104 developmental biologychemistryNeurotoxicity SyndromesLipid PeroxidationGeriatrics and GerontologybusinessAnaerobic exercise030217 neurology & neurosurgeryOxidative stressJournal of Alzheimer's disease : JAD
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Lack of NG2 exacerbates neurological outcome and modulates glial responses after traumatic brain injury

2015

Traumatic brain injury (TBI) is a major cause of death and disability. The underlying pathophysiology is characterized by secondary processes including neuronal death and gliosis. To elucidate the role of the NG2 proteoglycan we investigated the response of NG2-knockout mice (NG2-KO) to TBI. Seven days after TBI behavioral analysis, brain damage volumetry and assessment of blood brain barrier integrity demonstrated an exacerbated response of NG2-KO compared to wild-type (WT) mice. Reactive astrocytes and expression of the reactive astrocyte and neurotoxicity marker Lcn2 (Lipocalin-2) were increased in the perilesional brain tissue of NG2-KO mice. In addition, microglia/macrophages with acti…

0301 basic medicinePathologymedicine.medical_specialtyMicrogliaTraumatic brain injurybusiness.industryNeurotoxicityPoison controlBrain damagemedicine.diseaseBlood–brain barrier03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyGliosisImmunologymedicineNeurogliamedicine.symptombusinessGlia
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Activation of microglia synergistically enhances neurodegeneration caused by MPP+ in human SH-SY5Y cells

2019

While MPP+ may not directly activate microglia, the initial neuronal damage inflicted by the toxin may trigger microglia, possibly leading to synergistic pro-apoptotic interaction between neuro-inflammation and toxin-induced neurotoxicity, which may further aggravate neurodegeneration. However, what molecular targets are synergistically up or downregulated during this interaction is not well understood. Here, we addressed this by co-culturing fully differentiated human SH-SY5Y cells treated with parkinsonian toxin 1-Methyl-4-phenylpyridinium (MPP+), with endotoxin-activated microglial cell line EOC 20 to determine how this interaction affects pro-apoptotic (p38, JNK, and bax:bcl2 ratios) an…

0301 basic medicinePharmacologySH-SY5YMicrogliaChemistryp38 mitogen-activated protein kinasesNeurodegenerationNeurotoxicityInflammationmedicine.diseaseCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureApoptosismedicineViability assaymedicine.symptom030217 neurology & neurosurgeryEuropean Journal of Pharmacology
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Neurotoxicity of zearalenone’s metabolites and beauvericin mycotoxins via apoptosis and cell cycle disruption

2021

Cell cycle progression and programmed cell death are imposed by pathological stimuli of extrinsic or intrinsic including the exposure to neurotoxins, oxidative stress and DNA damage. All can cause abrupt or delayed cell death, inactivate normal cell survival or cell death networks. Nevertheless, the mechanisms of the neuronal cell death are unresolved. One of the cell deaths triggers which have been wildly studied, correspond to mycotoxins produced by Fusarium species, which have been demonstrated cytotoxicity and neurotoxicity through impairing cell proliferation, gene expression and induction of oxidative stress. The aim of present study was to analyze the cell cycle progression and cell …

0301 basic medicineProgrammed cell deathCellPopulationApoptosisToxicology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDepsipeptidesmedicineHumansEstrogens Non-SteroidaleducationCell Proliferationeducation.field_of_studyCell growthCell CycleNeurotoxicityMycotoxinsCell cyclemedicine.diseaseMolecular biologyBeauvericin030104 developmental biologymedicine.anatomical_structurechemistryApoptosisZearalenone030217 neurology & neurosurgeryToxicology
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