Search results for "lcsh:RC346-429"

showing 10 items of 162 documents

Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles

2019

Background Current evidence indicates that extracellular vesicles (EVs) participate in intercellular signaling, and in the regulation and amplification of neuroinflammation. We have previously shown that ethanol activates glial cells through Toll-like receptor 4 (TLR4) by triggering neuroinflammation. Here, we evaluate if ethanol and the TLR4 response change the release and inflammatory content of astrocyte-derived EVs, and whether these vesicles are capable of communicating with neurons by spreading neuroinflammation. Methods Cortical neurons and astrocytes in culture were used. EVs were isolated from the extracellular medium of the primary culture of the WT and TLR4-KO astrocytes treated …

0301 basic medicineImmunologyInflammationlcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineWestern blotNeuroinflammationGlial cellsExtracellularmedicineAnimalsProtein Interaction MapsReceptorNeuroinflammationCells Culturedlcsh:Neurology. Diseases of the nervous systemInflammationMice KnockoutNeuronsmedicine.diagnostic_testEthanolChemistryGeneral NeuroscienceResearchExtracellular vesiclesCell biologyMice Inbred C57BLToll-Like Receptor 4030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTLR4medicine.symptom030217 neurology & neurosurgeryIntracellularAstrocyteJournal of Neuroinflammation
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Deep Brain Stimulation and L-DOPA Therapy: Concepts of Action and Clinical Applications in Parkinson's Disease.

2018

L-DOPA is still the most effective pharmacological therapy for the treatment of motor symptoms in Parkinson's disease (PD) almost four decades after it was first used. Deep brain stimulation (DBS) is a safe and highly effective treatment option in patients with PD. Even though a clear understanding of the mechanisms of both treatment methods is yet to be obtained, the combination of both treatments is the most effective standard evidenced-based therapy to date. Recent studies have demonstrated that DBS is a therapy option even in the early course of the disease, when first complications arise despite a rigorous adjustment of the pharmacological treatment. The unique feature of this therapeu…

0301 basic medicineLevodopaParkinson's diseaseDeep brain stimulationglobus pallidus internus (GPi)medicine.medical_treatmentParkinson's diseaseCentral nervous systemStimulationDiseaseReviewlcsh:RC346-42903 medical and health sciencesTherapeutic approach0302 clinical medicinemedicinelevodopadeep brain stimulation (DBS)lcsh:Neurology. Diseases of the nervous systembusiness.industryDopaminergicmedicine.diseasenervous system diseases030104 developmental biologymedicine.anatomical_structureNeurologyNeurology (clinical)businessNeurosciencesubthalamic nucleus (STN)030217 neurology & neurosurgerymedicine.drugFrontiers in neurology
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Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.

2017

Background Adult neurogenesis persists through life at least in classic neurogenic niches. Neurogenesis has been previously described as reduced in neurodegenerative diseases. There is not much knowledge about is adult neurogenesis is or not modified in amyotrophy lateral sclerosis (ALS). All previous publications has studied the ALS SOD1 (superoxide dismutase) transgenic mouse model. The purpose of this study is to examine the process of adult neurogenesis in classic niches (subventricular zone [SVZ] and subgranular zone [SGZ] of the dentate gyrus) in patients with amyotrophic lateral sclerosis (ALS), both with (ALS-FTD) and without associated frontotemporal dementia (FTD). Methods We stud…

0301 basic medicineMalePathologymedicine.medical_specialtyDoublecortin ProteinTDP-43NeurogenesisSOD1Subventricular zoneAdult neurogenesislcsh:RC346-429Subgranular zone03 medical and health sciences0302 clinical medicineNeuroblastNeural Stem CellsLateral VentriclesMedicineHumansAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemAgedAged 80 and overbusiness.industryDentate gyrusNeurogenesisAmyotrophic Lateral SclerosisNeurodegenerative diseasesBrainGeneral MedicineMiddle Agedmedicine.diseaseNeural stem cellnervous system diseases030104 developmental biologymedicine.anatomical_structurenervous systemFrontotemporal DementiaFemaleNeurology (clinical)business030217 neurology & neurosurgeryResearch ArticleBMC neurology
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Myelin changes in Alexander disease

2018

Introduction: Alexander disease (AxD) is a type of leukodystrophy. Its pathological basis, along with myelin loss, is the appearance of Rosenthal bodies, which are cytoplasmic inclusions in astrocytes. Mutations in the gene coding for glial fibrillary acidic protein (GFAP) have been identified as a genetic basis for AxD. However, the mechanism by which these variants produce the disease is not understood. Development: The most widespread hypothesis is that AxD develops when a gain-of-function mutation causes an increase in GFAP. However, this mechanism does not explain myelin loss, given that experimental models in which GFAP expression is normal or mutated do not exhibit myelin disorders. …

0301 basic medicineMutationGlial fibrillary acidic proteinbiologyMechanism (biology)Cytoplasmic inclusionLeukodystrophymedicine.diseasemedicine.disease_causelcsh:RC346-429Alexander diseaseCell biology03 medical and health sciencesMyelin030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systembiology.proteinmedicineEpigeneticslcsh:Neurology. Diseases of the nervous system030217 neurology & neurosurgeryNeurología (English Edition)
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PPMS onset upon adalimumab treatment extends the spectrum of anti-TNF-α therapy-associated demyelinating disorders

2020

Since their introduction in 1999, anti-tumour necrosis factor-α (anti-TNF-α) therapies have been suspected repeatedly to be associated with the occurrence of central nervous system (CNS) demyelinating disorders, including multiple sclerosis (MS). However, recent publications were restricted to descriptions of monophasic demyelinating events or cases of relapsing–remitting MS (RRMS). We here provide the first case report of primary progressive MS (PPMS) onset upon anti-TNF-α therapy as well as a literature review of previously published cases of anti-TNF-α therapy-associated MS onset. The 51-year old male patient was treated with adalimumab due to psoriasis arthritis. About 18 months after …

0301 basic medicineNecrosisCentral nervous systemprimary progressive multiple sclerosisPrimary Progressive Multiple SclerosisCase ReportAnti-TNF-alpha therapylcsh:RC346-42903 medical and health sciences0302 clinical medicineadalimumabmedicineAdalimumabanti-TNF-alpha therapyDemyelinating DisorderAnti tnf α therapylcsh:Neurology. Diseases of the nervous systemPharmacologybusiness.industry030104 developmental biologymedicine.anatomical_structureNeurologyImmunologyNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgerymedicine.drugTherapeutic Advances in Neurological Disorders
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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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