Search results for "Astrogliosis"

showing 4 items of 14 documents

Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
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Cytopathologic and neurochemical correlates of progression to motor/cognitive impairment in SIV-infected rhesus monkeys.

1994

Neurochemical, pathologic, virologic, and histochemical correlates of simian immunodeficiency virus (SIV)-associated central nervous system (CNS) dysfunction were assessed serially or at necropsy in rhesus monkeys that exhibited motor and cognitive deficits after SIV infection. Some infected monkeys presented with signs of acquired immunodeficiency disease (AIDS) at the time of sacrifice. Seven of eight animals exhibited motor skill impairment which was associated with elevated quinolinic acid in cerebrospinal fluid (CSF). Examination of the brains revealed diffuse increases in glial fibrillary acidic protein immunoreacti vity in cerebral cortex in all animals, regardless of evidence of imm…

MalevirusesCentral nervous systemSimian Acquired Immunodeficiency SyndromeMotor Activitymedicine.disease_causeVirusPathology and Forensic MedicineCentral nervous system diseaseCellular and Molecular Neurosciencechemistry.chemical_compoundCerebrospinal fluidCognitionGlial Fibrillary Acidic ProteinmedicineAnimalsCerebral CortexGlial fibrillary acidic proteinbiologyBrainGeneral MedicineSimian immunodeficiency virusQuinolinic Acidmedicine.diseaseMacaca mulattaAstrogliosismedicine.anatomical_structureNeurologychemistrySpinal CordImmunologybiology.proteinSimian Immunodeficiency VirusNeurology (clinical)PsychologyCognition DisordersQuinolinic acidJournal of neuropathology and experimental neurology
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Neuronal injury in chronic CNS inflammation.

2010

Introduction Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system which is characterized by inflammatory demyelination and neurodegeneration. Neurological symptoms include sensory disturbances, optic neuritis, limb weakness, ataxia, bladder dysfunction, cognitive deficits and fatigue. Pathophysiology The inflammation process with MS is promoted by several inflammatory cytokines produced by the immune cells themselves and local resident cells like activated microglia. Consecutive damaging pathways involve the transmigration of activated B lymphocytes and plasma cells, which synthesize antibodies against the myelin sheath, boost the immune atta…

Multiple SclerosisInflammationNeuroprotectionSeverity of Illness IndexProinflammatory cytokineCentral Nervous System DiseasesmedicineAnimalsHumansRemyelinationNeuroinflammationInflammationNeuronsMicrogliabusiness.industryMultiple sclerosismedicine.diseaseAstrogliosisAnesthesiology and Pain Medicinemedicine.anatomical_structureNeuroprotective AgentsImmunologyChronic DiseaseMicrogliamedicine.symptomInflammation MediatorsbusinessBest practiceresearch. Clinical anaesthesiology
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Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice.

2014

Mechanisms underlying central neuropathic pain are poorly understood. Although glial dysfunction has been functionally linked with neuropathic pain, very little is known about modulation of pain by oligodendrocytes. Here we report that genetic ablation of oligodendrocytes rapidly triggers a pattern of sensory changes that closely resemble central neuropathic pain, which are manifest before overt demyelination. Primary oligodendrocyte loss is not associated with autoreactive T- and B-cell infiltration in the spinal cord and neither activation of microglia nor reactive astrogliosis contribute functionally to central pain evoked by ablation of oligodendrocytes. Instead, light and electron micr…

NociceptionSpinothalamic tractSpinal Cord Dorsal HornSpinothalamic TractsT-LymphocytesGeneral Physics and AstronomyAdaptive ImmunityGeneral Biochemistry Genetics and Molecular BiologyArticleMicemedicineAnimalsOligodendrocyte; central painB-LymphocytesMultidisciplinaryMicrogliabusiness.industryGeneral Chemistrymedicine.diseaseSpinal cordOligodendrocyteAxonsImmunity InnateAstrogliosisMicroscopy ElectronOligodendrogliamedicine.anatomical_structureNociceptionSpinal CordAstrocytesNeuropathic painNeuralgiaNeuralgiaMicrogliabusinessNeuroscienceNature communications
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