Search results for "nerve degeneration"

showing 10 items of 62 documents

Characterization of the cortical laser-doppler flow and hippocampal degenerative patterns after global cerebral ischaemia in the goat.

1998

Large-animal models offer several advantages in the study of cerebral ischaemia: easier control of physiological variables, easier neuropathological evaluation, etc. In the present study we have taken advantage of the unique cerebrovascular anatomy of the goat to reproduce a model of reversible, incomplete, global cerebral ischaemia in a large-sized animal species, in which the effects of successive manoeuvres to stop and re-start cerebral blood flow can be recorded continuously. Early cortical laser-Doppler flow response (up to 2 h) and delayed neuronal degeneration (7 days) in the hippocampal CA1 subfield have been analysed in goats undergoing 5, 10 or 20 min of transient, global cerebral…

Carotid Artery DiseasesTime FactorsPhysiologyClinical BiochemistryExternal carotid arteryIschemiaArterial Occlusive DiseasesHyperemiaHippocampusHyperaemiaPhysiology (medical)medicine.arteryOcclusionmedicineLaser-Doppler FlowmetryAnimalsIntracranial pressureCell Deathbusiness.industryGoatsPyramidal CellsHemodynamicsElectroencephalographymedicine.diseaseBlood pressureCerebral blood flowIschemic Attack TransientAnesthesiaCerebrovascular CirculationNerve DegenerationReperfusionFemalemedicine.symptombusinessPerfusionPflugers Archiv : European journal of physiology
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Membrane protein oxidation determines neuronal degeneration

2015

Oxidative stress is an early hallmark in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. However, the critical biochemical effector mechanisms of oxidative neurotoxicity have remained surprisingly elusive. In screening various peroxides and potential substrates of oxidation for their effect on neuronal survival, we observed that intramembrane compounds were significantly more active than aqueous or amphiphilic compounds. To better understand this result, we synthesized a series of competitive and site-specific membrane protein oxidation inhibitors termed aminoacyllipids, whose structures were designed on the basis of amino acids frequently found at the protein-lipi…

Cell SurvivalBiologyProtein oxidationmedicine.disease_causeBiochemistryProtein Structure SecondaryRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineAnimalsLipid bilayerCells CulturedNeuronsSphingosineNeurodegenerationNeurotoxicityMembrane Proteinsmedicine.diseaseTransmembrane proteinRatsCell biologyOxidative StressMembrane proteinchemistryNerve DegenerationReactive Oxygen SpeciesOxidation-ReductionOxidative stressJournal of Neurochemistry
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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Loss of input from the mossy cells blocks maturation of newly generated granule cells.

2007

The objective of this work is to check whether the input from the mossy cells to the inner molecular layer is necessary for the integration and maturation of the newly generated granule cells of the dentate gyrus (DG) in mice, and if after status epilepticus the sprouting of the mossy fibers can substitute for this projection. Newly generated cells were labeled by administration of 5-bromo-deoxyuridine either before or after pilocarpine administration. The neuronal loss in the hippocampus after administration of pilocarpine combined with scopolamine and diazepam seemed restricted to the hilar mossy cells. The maturation of the granule cells was studied using immunohistochemistry for calreti…

Cell typeCell SurvivalCognitive NeuroscienceScopolamineConvulsantsNerve Tissue ProteinsMuscarinic Antagonistschemistry.chemical_compoundMiceS100 Calcium Binding Protein GStatus EpilepticusmedicineAnimalsCell ProliferationDiazepamEpilepsyNeuronal PlasticitybiologyChemistryDentate gyrusStem CellsGranule (cell biology)PilocarpineNuclear ProteinsCell DifferentiationImmunohistochemistryDNA-Binding Proteinsnervous systemBromodeoxyuridinePilocarpineCalbindin 2Dentate GyrusMossy Fibers HippocampalNerve Degenerationbiology.proteinAnticonvulsantsFemaleNeuNCalretininNeuroscienceBromodeoxyuridineBiomarkersSproutingmedicine.drugHippocampus
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Molecular mechanisms linking neuroinflammation and neurodegeneration in MS.

2013

Multiple sclerosis (MS) is an inflammatory demyelinating autoimmune disorder of the central nervous system (CNS) and one of the leading causes of neurological deficits and disability in young adults in western countries. Current medical treatment mainly influences disease progression via immunomodulatory or immunosuppressive actions. Indeed, MS research has been foremost focused on inflammation in the CNS, but more recent evidence suggests that chronic disability in MS is caused by neurodegeneration. Imaging studies show an early involvement of neurodegeneration as brain atrophy and gray matter lesions can be observed at disease onset. Thus, neuroprotective treatment strategies and the eluc…

Central Nervous SystemMultiple SclerosisCentral nervous systemBiologyNeuroprotectionPathogenesisAtrophyDevelopmental NeurosciencemedicineAnimalsHumansImmunologic FactorsNeuroinflammationInflammationMultiple sclerosisExperimental autoimmune encephalomyelitisNeurodegenerationmedicine.diseaseDisease Models Animalmedicine.anatomical_structureNeurologyImmunologyNerve DegenerationDisease ProgressionCytokinesNeuroscienceExperimental neurology
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Quantitative image analysis of the chromatolysis in rat facial and hypoglossal motoneurons following axotomy with and without reinnervation.

1996

Image analysis was used to quantify the time course of chromatolysis in regenerating and degenerating motoneurons. Following facial-facial, hypoglossal-hypoglossal nerve suture, or resection of facial and hypoglossal nerves with postoperative survival times of 4 h to 112 days, the texture of the Nissl substance of facial and hypoglossal motoneurons was analyzed on both sides of the brainstem in paraffin serial sections with a VIDASplus image analyzer. In this quantitative study of 149 Wistar rats, alterations of the Nissl substance were measured that were statistically significant but not yet visible to the human eye. Chromatolysis started significantly as early as 8 h and was not fully rev…

Hypoglossal NerveHistologyTime Factorsmedicine.medical_treatmentPathology and Forensic Medicinesymbols.namesakemedicineImage Processing Computer-AssistedAnimalsRats WistarMotor Neuronsbusiness.industryCell BiologyAnatomyFacial nerveAxonsNerve RegenerationRatsFacial Nervemedicine.anatomical_structurenervous systemNissl BodiesChromatolysisTime courseNerve DegenerationNissl bodysymbolsFemaleBrainstemAxotomybusinessHypoglossal nerveReinnervationCell and tissue research
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Phenothiazines interfere with dopaminergic neurodegeneration in Caenorhabditis elegans models of Parkinson's disease

2010

Oxidative stress is involved in the pathogenesis of various neurodegenerative disorders, conventional antioxidant strategies have yet been of limited success. We have employed transgenic Caenorhabditis elegans expressing DsRed2 in dopaminergic neurons and CFP pan-neuronally, to characterize in larval and adult animals the effects of rotenone and 1-methyl-4-phenyl-pyridinium (MPP(+)) on the dopaminergic system. Investigating the antioxidant phenothiazine and different derived antipsychotic drugs, it was found that free phenothiazine exerted strong neuroprotection at the cellular level and resulted in a better performance in behavioral assays, whereas apomorphine and other dopamine agonists o…

InsecticidesApomorphineChlorpromazineDopamineBiologyPharmacologyNeuroprotectionlcsh:RC321-571Animals Genetically Modifiedchemistry.chemical_compoundAntipsychotic drugParkinsonian DisordersDopaminePhenothiazinesRotenonemedicineAnimalsHumansChlorpromazineCaenorhabditis eleganslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationNeuronsDopaminergic neuronModels GeneticNeurodegenerationDopaminergicRotenonemedicine.diseaseDisease Models AnimalNeuroprotective AgentsNeurologychemistryDopamine receptorNerve DegenerationAntioxidantTricyclicmedicine.drugAntipsychotic AgentsNeurobiology of Disease
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A Natural Dietary Supplement with a Combination of Nutrients Prevents Neurodegeneration Induced by a High Fat Diet in Mice

2018

Obesity and metabolic disorders can be risk factors for the onset and development of neurodegenerative diseases. The aim of the present study was to investigate the protective effects of a natural dietary supplement (NDS), containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin, on dysmetabolism and neurodegeneration in the brains of high fat diet (HFD)-fed mice. Decrease in the expression of FACL-4, CerS-1, CerS-4, cholesterol concentration and increase in the insulin receptor expression and insulin signaling activation, were found in brains of NDS-treated HFD brains in comparison with HFD untreated-mice, suggesting that NDS is able to prevent brain lipid accumulation and …

Male0301 basic medicineobesityAntioxidantmedicine.medical_treatmentAnti-Inflammatory AgentsApoptosismedicine.disease_causeSettore BIO/09 - FisiologiaAntioxidantsLipid peroxidationchemistry.chemical_compound0302 clinical medicineinsulin resistanceInsulinnatural antioxidantsNutrition and DieteticsbiologyChemistryneurodegenerationobesity; HFD mice; natural antioxidants; insulin resistance; neurodegenerationBrainfood and beveragesNeurodegenerative Diseaseslipids (amino acids peptides and proteins)Inflammation Mediatorsmedicine.symptomlcsh:Nutrition. Foods and food supplySignal Transductionmedicine.medical_specialtylcsh:TX341-641endocrinology_metabolomicsInflammationDiet High-FatNeuroprotectionArticle03 medical and health sciencesInsulin resistanceInternal medicinemedicineAnimalsHFD miceCholesterolInsulinLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressInsulin receptor030104 developmental biologyEndocrinologyDietary SupplementsNerve Degenerationbiology.proteinLipid Peroxidationnatural antioxidant030217 neurology & neurosurgeryOxidative stressFood ScienceNutrients
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Aspirin protects striatal dopaminergic neurons from neurotoxin-induced degeneration: an in vivo microdialysis study.

2006

The effect of aspirin on dopaminergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) and 6-hydroxydopamine (6-OHDA) was studied in rats, using microdialysis. Rat striata were perfused with 1 mM MPP(+) or 6-OHDA for 10 min, causing peak levels of dopamine (DA) in the dialytic fluid, after 40 min. After 24 h, 1 mM MPP(+) was perfused again for 10 min and DA levels measured in the dialytic fluid, as an index of neuronal cell integrity. Pretreatment with Aspidol (lysine acetylsalicylate), 180 mg/kg i.p., 1 h before MPP(+) or 6-OHDA perfusion, did not modify DA extracellular output, on day 1, but restored MPP(+)-induced DA release on day 2, indicating …

MaleMicrodialysisTyrosine 3-MonooxygenaseDopamineMicrodialysisNeurotoxinsPharmacologyNeuroprotectionSettore BIO/09 - FisiologiaRats Sprague-Dawleychemistry.chemical_compoundIn vivoHydroxybenzoatesNeurotoxinAnimalsDrug InteractionsMolecular BiologyChromatography High Pressure LiquidNeuronsAnalysis of VarianceAspirinGeneral NeuroscienceMPTPDopaminergicImmunohistochemistryCorpus StriatumRatsNeuroprotective Agentsnervous systemchemistryAnesthesiaNerve DegenerationNeurology (clinical)Aspirin in vivo microdialysisPerfusionOxidopamineDevelopmental Biology
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Mild Hypothermia Has No Long-Term Impact on Postischemic Neurogenesis in Rats

2009

Postischemic improvement of functional outcome by therapeutic hypothermia may be related to cerebral regeneration by postischemic neurogenesis. We investigated whether mild peri-ischemic hypothermia leads to a long-term increase in postischemic neurogenesis.Seventy male sevoflurane-anesthetized Sprague Dawley rats were randomly assigned to the following treatment groups: normothermic ischemia, intraischemic hypothermia, and postischemic hypothermia with corresponding sham-operated controls. Fifteen naïve rats were investigated as reference for natural neurogenesis. Forebrain ischemia was induced by bilateral common carotid artery occlusion and hemorrhagic hypotension. In normothermic groups…

MaleMild hypothermiaTime FactorsNeurogenesisIschemiaSeverity of Illness IndexBrain IschemiaRats Sprague-DawleyProsencephalonHypothermia InducedmedicineAnimalsCell ProliferationNeuronsbusiness.industryNeurogenesisHypothermiamedicine.diseaseRatsSprague dawleyDisease Models AnimalAnesthesiology and Pain MedicineAnesthesiaDentate GyrusNerve Degenerationmedicine.symptombusinessAnesthesia & Analgesia
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