Search results for "346"

showing 10 items of 252 documents

The Impacts of Tumor and Tumor Associated Epilepsy on Subcortical Brain Structures and Long Distance Connectivity in Patients With Low Grade Glioma

2018

Low grade gliomas in cerebral cortex often cause symptoms related to higher cerebral functions such as attention, memory and executive function before treatment is initiated. Interestingly, focal tumors residing in one cortical region can lead to a diverse range of symptoms, indicating that the impact of a tumor is extended to multiple brain regions. We hypothesize that the presence of focal glioma in the cerebral cortex leads to alterations of distant subcortical areas and essential white matter tracts. In this study, we analyzed diffusion tensor imaging scans in glioma patients to study the effect of glioma on subcortical gray matter nuclei and long-distance connectivity. We found that th…

0301 basic medicinePathologymedicine.medical_specialtyBrain tumorlcsh:RC346-429White matter03 medical and health sciences0302 clinical medicinegliomaGliomamedicinelcsh:Neurology. Diseases of the nervous systemOriginal Researchtumor associated epilepsybusiness.industrydiffusion tensor imagingmedicine.diseaseSubcortical gray matter030104 developmental biologymedicine.anatomical_structureNeurologyCerebral cortexconnectivityCerebellar cortexNeurology (clinical)business030217 neurology & neurosurgeryMRIDiffusion MRITractography
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Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute experimental tr…

2019

Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate the hitherto unresolved role of immunosuppressive, regulatory T cells (Tregs) in experimental TBI. Methods “Depletion of regulatory T cell” (DEREG) and wild type (WT) C57Bl/6 mice, treated with diphtheria toxin (DTx) to deplete Tregs or to serve as control, were subjected to the controlled cortical impact (CCI) model of TBI. Neurological and motor deficits were examined until 5 days post-injury (dpi). At the 5 dpi endpoint, (immuno-) histological…

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injuryRegulatory T cellT cellImmunologyT cellsExcitotoxicityBrain damagemedicine.disease_causelcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceTraumatic brain injury0302 clinical medicinemedicineImmune responselcsh:Neurology. Diseases of the nervous systemInflammationGlial fibrillary acidic proteinbiologybusiness.industryResearchGeneral Neurosciencemedicine.diseaseAstrogliosisCD8A030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesbiology.proteinCytokinesMicrogliamedicine.symptombusiness030217 neurology & neurosurgeryJournal of Neuroinflammation
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Non-Rapid Eye Movement Sleep Parasomnias and Migraine: A Role of Orexinergic Projections

2018

Introduction: Sleep and migraine share a common pathophysiological substrate, although the underlying mechanisms are unknown. The serotonergic and orexinergic systems are both involved in the regulation of sleep/wake cycle, and numerous studies show that both are involved in the migraine etiopathogenesis. These two systems are anatomically and functionally interconnected. Our hypothesis is that in migraine a dysfunction of orexinergic projections on the median raphe (MR) nuclei, interfering with serotonergic regulation, may cause Non-Rapid Eye Movement parasomnias, such as somnambulism. Hypothesis/theory: Acting on the serotonergic neurons of the raphe nuclei, the dysfunction of orexinergic…

0301 basic medicineSerotonergic systemMigraine; Orexinergic system; Pro-inflammatory peptides; Serotonergic system; Sleep-wake rhythm; Neurology; Neurology (clinical)Substance PCalcitonin gene-related peptidePro-inflammatory peptideSerotonergicNon-rapid eye movement sleeplcsh:RC346-429sleep–wake rhythmMigraine; Orexinergic system; Pro-inflammatory peptides; Serotonergic system; Sleep-wake rhythm;Settore M-PSI/04 - Psicologia Dello Sviluppo E Psicologia Dell'Educazione03 medical and health sciencesTrigeminal ganglionchemistry.chemical_compound0302 clinical medicinePro-inflammatory peptidesSleep-wake rhythmHypothesis and TheoryMedicinelcsh:Neurology. Diseases of the nervous systemMigraineMigraine; Orexinergic system; Pro-inflammatory peptides; Serotonergic system; Sleep-wake rhythmbusiness.industryOrexinergic systemserotonergic system orexinergic system sleep–wake rhythm migraine pro-inflammatory peptidesSettore MED/39 - Neuropsichiatria InfantileOrexin030104 developmental biologyNeurologychemistryNeurology (clinical)SerotoninbusinessRaphe nucleiNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Neurology
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Cellular Response to Spinal Cord Injury in Regenerative and Non-Regenerative Stages in Xenopus Laevis

2020

Abstract Background The efficient regenerative abilities at larvae stages followed by a non-regenerative response after metamorphosis in froglets makes Xenopus an ideal model organism to understand the cellular responses leading to spinal cord regeneration. Methods We compared the cellular response to spinal cord injury between the regenerative and non-regenerative stages of Xenopus laevis. For this analysis, we used electron microscopy, immunofluorescence and histological staining of the extracellular matrix. We generated two transgenic lines: i) the reporter line with the zebrafish GFAP regulatory regions driving the expression of EGFP, and ii) a cell specific inducible ablation line with…

0301 basic medicineSpinal Cord RegenerationGfapXenopusNeurogenesislcsh:RC346-429Glial scarGlial scar03 medical and health sciencesXenopus laevis0302 clinical medicineDevelopmental NeuroscienceNeural Stem CellsmedicineAnimalsRegenerationsox2Progenitor cellSpinal cord injuryZebrafishSpinal Cord RegenerationSpinal Cord InjuriesZebrafishlcsh:Neurology. Diseases of the nervous systemSpinal cordbiologyRegeneration (biology)NeurogenesisSpinal cordmedicine.diseasebiology.organism_classificationCell biology030104 developmental biologymedicine.anatomical_structureNSPCsnervous system030217 neurology & neurosurgeryResearch Article
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Retinal Thickness and Microvascular Pattern in Early Parkinson's Disease.

2020

A thinning of intraretinal layers has been previously described in Parkinson's disease (PD) patients compared to healthy controls (HCs). Few studies evaluated the possible correlation between retinal thickness and retinal microvascularization. Thus, here we assessed the thickness of retinal layers and microvascular pattern in early PD patients and HCs, using, respectively, spectral-domain optical coherence tomography (SD-OCT) and SD-OCT-angiography (SD-OCT-A), and more interestingly, we evaluated a possible correlation between retinal thickness and microvascular pattern. Patients fulfilling criteria for clinically established/clinically probable PD and HCs were enrolled. Exclusion criteria …

0301 basic medicineSystemic diseasemedicine.medical_specialtyretinaParkinson's diseasegenetic structuresNerve fiber layeroptical coherence tomography angiographylcsh:RC346-42903 medical and health scienceschemistry.chemical_compound0302 clinical medicinevascularizationOphthalmologyMedicinelcsh:Neurology. Diseases of the nervous systemOriginal ResearchRetinaoptical coherence tomographybusiness.industryMicrovascular DensityRetinalmedicine.diseaseInner plexiform layereye diseases030104 developmental biologymedicine.anatomical_structurechemistryNeurologyInner nuclear layerparkinson's diseaseNeurology (clinical)sense organsbusiness030217 neurology & neurosurgeryoptical coherence tomography; optical coherence tomography angiography; parkinson's disease; retina; vascularizationFrontiers in neurology
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Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer’s disease

2018

Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or …

0301 basic medicineTime Factorsmedicine.medical_treatmentHippocampusCell CountPharmacologymedicine.disease_causeHippocampuslcsh:RC346-429Superoxide Dismutase-10302 clinical medicineNeuroinflammationNF-kBMicrogliaGeneral NeuroscienceMicrofilament ProteinsROSPro-inflammatory cytokineIFNβ1amedicine.anatomical_structureCytokineNeurologyIL-10CytokinesFemalemedicine.symptomAlzheimer's diseaseInterferon beta-1aPro-inflammatory cytokinesImmunologyAβ 1-42InflammationProinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceHippocampuAlzheimer DiseaseGlial Fibrillary Acidic ProteinmedicineAnimalsAβ1-42Rats WistarSODMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationInflammationAmyloid beta-PeptidesNeuroscience (all)Superoxide Dismutasebusiness.industryResearchCalcium-Binding ProteinsRecognition Psychologymedicine.diseasePeptide FragmentsRatsDisease Models Animal030104 developmental biologyLipid PeroxidationCognition DisordersReactive Oxygen Speciesbusiness030217 neurology & neurosurgeryOxidative stressJournal of Neuroinflammation
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Neurostimulation and Reach-to-Grasp Function Recovery Following Acquired Brain Injury: Insight From Pre-clinical Rodent Models and Human Applications.

2020

Reach-to-grasp is an evolutionarily conserved motor function that is adversely impacted following stroke and traumatic brain injury (TBI). Non-invasive brain stimulation (NIBS) methods, such as transcranial magnetic stimulation and transcranial direct current stimulation, are promising tools that could enhance functional recovery of reach-to-grasp post-brain injury. Though the rodent literature provides a causal understanding of post-injury recovery mechanisms, it has had a limited impact on NIBS protocols in human research. The high degree of homology in reach-to-grasp circuitry between humans and rodents further implies that the application of NIBS to brain injury could be better informed…

0301 basic medicineTraumatic brain injurymedicine.medical_treatmentReviewlcsh:RC346-42903 medical and health sciences0302 clinical medicinemedicineReach to grasphumanNeurostimulationAcquired brain injuryNeurorehabilitationlcsh:Neurology. Diseases of the nervous systemTranscranial direct-current stimulationreach-and-graspbusiness.industrytraumatic brain injuryrodentmedicine.diseasestrokeTranscranial magnetic stimulation030104 developmental biologyNeurologyBrain stimulationneuromodulationNeurology (clinical)businessNeuroscience030217 neurology & neurosurgeryFrontiers in neurology
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Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC

2019

Seventy years of research on Western Pacific amyotrophic lateral sclerosis and Parkinsonism-dementia Complex (ALS/PDC) have provided invaluable data on the etiology, molecular pathogenesis and latency of this disappearing, largely environmental neurodegenerative disease. ALS/PDC is linked to genotoxic chemicals (notably methylazoxymethanol, MAM) derived from seed of the cycad plant (Cycas spp.) that were used as a traditional food and/or medicine in all three disease-affected Western Pacific populations. MAM, nitrosamines and hydrazines generate methyl free radicals that damage DNA (in the form of O6-methylguanine lesions) that can induce mutations in cycling cells and degenerative changes …

0301 basic medicineamyotrophic lateral sclerosisDNA damageDiseaseBiologylcsh:RC346-429Environmental - originProgressive supranuclear palsy03 medical and health sciences0302 clinical medicineHypothesis and TheorymedicinenitrosaminesAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemhydrazinesprogressive supranuclear palsymedicine.diseaseatypical parkinsonism030104 developmental biologyBrain degenerationNeurologyImmunologyEtiologycycad methylazoxymethanol and L-BMAADNA damageNeurology (clinical)Alzheimer's diseaseAlzheimer disease030217 neurology & neurosurgeryFrontiers in Neurology
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Extrinsic and intrinsic mechanisms of axon regeneration: the need for spinal cord injury treatment strategies to address both

2016

Spinal cord injury (SCI) causes disturbances in motor and sensory functions leading to paralysis, the severity of which depends on the spinal level of the injury. Traumatic lesions of spinal cord axon projection tracts are untreatable in human patients, although numerous research groups worldwide are studying putative treatment strategies. Both extrinsic factors in the environment of the axons as well as intrinsic factors in the neurons themselves play important roles in the regeneration process (Chew et al., 2012). The peripheral nervous system (PNS) provides a good example where the extrinsic and intrinsic factors play optimally together to allow regeneration. Schwann cells dedifferentiat…

0301 basic medicinebusiness.industryRegeneration (biology)Central nervous systemInhibitory postsynaptic potentialmedicine.diseaseSpinal cordlcsh:RC346-42903 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systemDevelopmental NeurosciencePeripheral nervous systemPerspectivemedicineAxonbusinessGrowth coneSpinal cord injuryNeurosciencelcsh:Neurology. Diseases of the nervous system030217 neurology & neurosurgeryNeural Regeneration Research
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Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differenti…

2017

Background Alexander disease (AxD) is a rare disease caused by mutations in the gene encoding glial fibrillary acidic protein (GFAP). The disease is characterized by presence of GFAP aggregates in the cytoplasm of astrocytes and loss of myelin. Objectives Determine the effect of AxD-related mutations on adult neurogenesis. Methods We transfected different types of mutant GFAP into neurospheres using the nucleofection technique. Results We find that mutations may cause coexpression of GFAP and NG2 in neurosphere cultures, which would inhibit the differentiation of precursors into oligodendrocytes and thus explain the myelin loss occurring in the disease. Transfection produces cells that diff…

0301 basic medicinecaspase-3Cathepsin Dmacromolecular substancesHSP27lcsh:RC346-429oligodendrocyte precursors03 medical and health sciencesMyelin0302 clinical medicineAlexander diseaseNG2Neurosphereneurospheresmedicinecathepsinlcsh:Neurology. Diseases of the nervous systemOriginal ResearchGlial fibrillary acidic proteinbiologyNeurogenesisNestinGFAP stainmedicine.diseaseMolecular biologyAlexander disease030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyglial fibrillary acidic proteinbiology.proteinNeurology (clinical)030217 neurology & neurosurgeryNeuroscienceFrontiers in Neurology
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