Search results for "nerve degeneration"

showing 10 items of 62 documents

DNA-fragmentation and apoptosis-related proteins of muscle cells in motor neuron disorders

2009

Apoptosis has been described as one of the mechanisms of muscle fiber loss in infantile spinal muscular atrophy. In order to investigate if muscle fiber-apoptosis plays a role in other denervating disorders as well, we studied DNA-fragmentation, a hallmark of apoptosis, by the TUNEL-method and, moreover, the expression patterns of apoptosis-related proteins in 2 patients suffering from ALS and in 6 patients with polyneuropathy. We identified DNA-cleavage in muscle fibers of all these patients. Furthermore, we found strong expression of bax and ICE promoting apoptosis in muscle fibers. However, also strong expression of the anti-apoptotic factor bcl-2 was found. Our findings indicate that de…

AdultMalePathologymedicine.medical_specialtyMuscle Fibers SkeletalApoptosisCell Cycle ProteinsDNA FragmentationBiologyProto-Oncogene ProteinsGene expressionmedicineHumansMyocytefas ReceptorMotor Neuron DiseaseAmyotrophic lateral sclerosisMuscle SkeletalActinAgedReceptors Leukocyte-AdhesionAmyotrophic Lateral SclerosisPeripheral Nervous System DiseasesGeneral MedicineMiddle AgedMotor neuronmedicine.diseaseCell biologyCysteine Endopeptidasesmedicine.anatomical_structureNeurologyApoptosisNerve DegenerationDNA fragmentationFemaleNeurology (clinical)AtrophyPolyneuropathyActa Neurologica Scandinavica
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The temporal dynamics of postanoxic burst-suppression EEG.

2002

Burst-suppression EEG (BS-EEG) after cardiopulmonary resuscitation implies a bad prognosis, but little is known of the temporal dynamics of postanoxic BS-EEG. The authors studied 24 consecutive patients who developed BS-EEG within 24 hours after cardiopulmonary resuscitation, and followed 20 of these patients with serial EEGs. Except for one patient, BS-EEG was followed by another EEG pattern within 1 day, mainly areactive alpha EEG (n = 6), isoelectric EEG (n = 5), generalized continuous epileptiform discharges (n = 4), or theta; EEG (n = 3). The coexistence of different EEG patterns in the same recording was seen in 10 patients. Serial recordings disclosed a variety of EEG sequences with …

AdultMalePhysiologyElectroencephalographyEEG-fMRIBrain diagnosisEeg patternsEpilepsyPhysiology (medical)medicineHumansIn patientHypoxia BrainEvoked PotentialsAgedCerebral CortexNeuronsmedicine.diagnostic_testElectroencephalographyMiddle Agedmedicine.diseasePrognosisCardiopulmonary ResuscitationBurst suppressionNeurologyAnesthesiaNerve DegenerationBrain Damage ChronicEpilepsy GeneralizedFemaleNeurology (clinical)Anoxic encephalopathyPsychologyNeuroscienceJournal of clinical neurophysiology : official publication of the American Electroencephalographic Society
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Effect of focal cerebellar lesions on procedural learning in the serial reaction time task

1998

Prior studies have shown that procedural learning is severely impaired in patients with diffuse cerebellar damage (cortical degeneration) as measured by the serial reaction time task (SRTT). We hypothesize that focal cerebellar lesions can also have lateralized effects on procedural learning. Our objective was to assess the effects of focal cerebellar lesions in procedural learning as measured by the SRTT. We studied 14 patients with single, unilateral vascular lesions in the territory of the posterior-inferior or superior cerebellar artery, who were compared with ten age- and sex-matched controls in a one-handed version of the SRTT. Patients with lesions at any other level of the brain or …

AdultMaleSerial reaction timemedicine.medical_specialtyCerebellumNeurologyCentral nervous systemProcedural memoryLesionCerebellar Diseasesmedicine.arteryReaction TimemedicineHumansLearningSuperior cerebellar arteryAgedAnalysis of Variancemedicine.diagnostic_testGeneral NeuroscienceReproducibility of ResultsMagnetic resonance imagingMiddle Agedmedicine.anatomical_structureCase-Control StudiesChronic DiseaseNerve DegenerationFemaleRadiologymedicine.symptomPsychologyNeurosciencePsychomotor PerformanceExperimental Brain Research
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Morphologic diagnosis in neuronal ceroid lipofuscinosis.

1997

Morphologic pathology in NCL is marked by two processes, the interaction of which has not yet been completely clarified: 1) degeneration of nerve cells, foremost in the cerebral cortex, resulting in considerable cerebral atrophy in early childhood forms, likely responsible for clinical and neuroradiological findings; 2) widespread accumulation of autofluorescent lysosomal lipopigments of varying ultrastructure, the demonstration of which is still largely responsible for diagnostic recognition of an individual patient's NCL. Numerous tissues and organs are available for biopsy, among them brain (historical), rectum (still favoured by some), skeletal muscle and peripheral nerves (largely by c…

AdultPathologymedicine.medical_specialtyConjunctivaAdolescentBiopsyAutopsyAtrophyNeuronal Ceroid-LipofuscinosesBiopsyMedicineHumansTissue DistributionChildCerebral atrophyCerebral Cortexmedicine.diagnostic_testbusiness.industryInfantGeneral MedicinePigments Biologicalmedicine.diseaseLipidsmedicine.anatomical_structureCerebral cortexChild PreschoolPediatrics Perinatology and Child HealthNerve DegenerationNeuronal ceroid lipofuscinosisNeurology (clinical)Morphologic diagnosisAtrophybusinessLysosomesNeuropediatrics
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Temporal Structure of Human Gaze Dynamics Is Invariant During Free Viewing.

2015

We investigate the dynamic structure of human gaze and present an experimental study of the frequency components of the change in gaze position over time during free viewing of computer-generated fractal images. We show that changes in gaze position are scale-invariant in time with statistical properties that are characteristic of a random walk process. We quantify and track changes in the temporal structure using a well-defined scaling parameter called the Hurst exponent, H. We find H is robust regardless of the spatial complexity generated by the fractal images. In addition, we find the Hurst exponent is invariant across all participants, including those with distinct changes to higher or…

AdultVisual acuityAdolescentEye MovementsComputer scienceInformationSystems_INFORMATIONINTERFACESANDPRESENTATION(e.g.HCI)ComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISIONVisual Acuitylcsh:MedicineNeural degenerationTemporal lobeOcular Motility DisordersYoung AdultFractalInformationSystems_MODELSANDPRINCIPLESOcular Motility DisordersMuscle Stretching ExercisesmedicineHumansComputer visionInvariant (mathematics)lcsh:ScienceHurst exponentMultidisciplinarybusiness.industrylcsh:REye movementComputational BiologyRandom walkGazeTemporal LobeFractalsHuman visual system modelNerve Degenerationlcsh:QArtificial intelligencemedicine.symptombusinessResearch ArticlePLoS ONE
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Impaired calcium homeostasis in aged hippocampal neurons

2009

Abstract Development of neurodegenerative diseases such as Alzheimer's and Parkinson's disease is strongly age-associated. The impairment of calcium homeostasis is considered to be a key pathological event leading to neuronal dysfunction and cell death. However, the exact impact of aging on calcium homeostasis in neurons remains largely unknown. In the present work we have investigated intracellular calcium levels in cultured primary hippocampal neurons from young (2 months) and aged (24 months) rat brains. Upon stimulation with glutamate or hydrogen peroxide aged neurons in comparison to young neurons demonstrated an increased vulnerability to these disease-related toxins. Measurement of c…

Agingmedicine.medical_specialtyNeurotoxinsGlutamic Acidchemistry.chemical_elementHippocampusBiologyCalciumHippocampusCalcium in biologyRats Sprague-DawleyInternal medicinemedicineAnimalsCalcium SignalingOrganic ChemicalsCells CulturedCellular SenescenceNeuronsCalcium metabolismCalpainGeneral NeuroscienceNeurodegenerationGlutamate receptorCalpainHydrogen PeroxideOxidantsmedicine.diseaseRatsOxidative Stressmedicine.anatomical_structureEndocrinologynervous systemchemistryNerve Degenerationbiology.proteinCalciumNeuronNeuroscienceNeuroscience Letters
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Novel imine antioxidants at low nanomolar concentrations protect dopaminergic cells from oxidative neurotoxicity.

2009

Strong evidence indicates that oxidative stress may be causally involved in the pathogenesis of Parkinson's disease. We have employed human dopaminergic neuroblastoma cells and rat primary mesencephalic neurons to assess the protective potential of three novel bisarylimine antioxidants on dopaminergic cell death induced by complex I inhibition or glutathione depletion. We have found that exceptionally low concentrations (EC(50) values approximately 20 nM) of these compounds (iminostilbene, phenothiazine, and phenoxazine) exhibited strong protective effects against the toxicities of MPP(+), rotenone, and l-buthionine sulfoximine. Investigating intracellular glutathione levels, it was found t…

Antioxidantmedicine.medical_treatmentDopamineGlutathione reductaseNeurotoxinsBiologymedicine.disease_causeProtein oxidationBiochemistryAntioxidantsLipid peroxidationRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumormedicineAnimalsHumansCells CulturedMembrane Potential MitochondrialCell DeathDose-Response Relationship DrugNeurotoxicityParkinson DiseaseRotenoneGlutathionemedicine.diseaseGlutathioneMitochondriaRatsSubstantia NigraOxidative StressNeuroprotective AgentschemistryBiochemistryElectron Transport Chain Complex ProteinsCytoprotectionNerve DegenerationIminesOxidation-ReductionOxidative stressJournal of neurochemistry
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Cross-recognition of a myelin peptide by CD8+ T cells in the CNS is not sufficient to promote neuronal damage.

2015

Multiple sclerosis (MS) is an inflammatory disease of the CNS thought to be driven by CNS-specific T lymphocytes. Although CD8+T cells are frequently found in multiple sclerosis lesions, their distinct role remains controversial because direct signs of cytotoxicity have not been confirmedin vivo. In the present work, we determined that murine ovalbumin-transgenic (OT-1) CD8+T cells recognize the myelin peptide myelin oligodendrocyte glycoprotein 40–54 (MOG40–54) bothin vitroandin vivo. The aim of this study was to investigate whether such cross-recognizing CD8+T cells are capable of inducing CNS damagein vivo. Using intravital two-photon microscopy in the mouse model of multiple sclerosis, …

CD4-Positive T-LymphocytesCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisAutoimmunityMice TransgenicCD8-Positive T-Lymphocytesmedicine.disease_causeMyelin oligodendrocyte glycoproteinMyelinMiceIn vivomedicineCytotoxic T cellAnimalsCells CulturedCell ProliferationbiologyCell DeathGeneral NeuroscienceMultiple sclerosisArticlesmedicine.diseaseMolecular mimicrymedicine.anatomical_structureImmunologyNerve Degenerationbiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinCD8Intravital microscopyThe Journal of neuroscience : the official journal of the Society for Neuroscience
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB(1)).

2012

Endocannabinoids exert numerous effects in the CNS under physiological and pathological conditions. The aim of the present study was to examine whether the endocannabinoid N-arachidonoyldopamine (NADA) may protect neurons in excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). OHSC were excitotoxically lesioned by application of N-methyl-d-aspartate (NMDA, 50 μM) for 4 h and subsequently treated with different NADA concentrations (0.1 pM-50 μM) alone or in combination with cannabinoid receptor antagonists. NADA protected dentate gyrus granule cells and caused a slight reduction in the number of microglial cells. The number of degenerated neurons significantly decreased be…

Cannabinoid receptorDopamineTRPV1Arachidonic AcidsPharmacologyNeuroprotectionHippocampusCellular and Molecular NeuroscienceMicePiperidinesReceptor Cannabinoid CB1Neuronal damageAnimalsRats WistarCells CulturedPharmacologyNeuronsChemistryDentate gyrusExcitatory Postsynaptic PotentialsEndocannabinoid systemRatsNeuroprotective Agentsnervous systemNerve DegenerationCannabinoid receptor antagonistNMDA receptorPyrazolesNeuropharmacology
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Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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