Search results for "C3"

showing 10 items of 1295 documents

Hypoxia in CNS Pathologies: Emerging Role of miRNA-Based Neurotherapeutics and Yoga Based Alternative Therapies

2017

Cellular respiration is a vital process for the existence of life. Any condition that results in deprivation of oxygen (also termed as hypoxia) may eventually lead to deleterious effects on the functioning of tissues. Brain being the highest consumer of oxygen is prone to increased risk of hypoxia-induced neurological insults. This in turn has been associated with many diseases of central nervous system (CNS) such as stroke, Alzheimer's, encephalopathy etc. Although several studies have investigated the pathophysiological mechanisms underlying ischemic/hypoxic CNS diseases, the knowledge about protective therapeutic strategies to ameliorate the affected neuronal cells is meager. This has au…

0301 basic medicineEncephalopathyCentral nervous systemIschemiaReviewischemiaBiologyNeuroprotectionlcsh:RC321-571breathing exercise03 medical and health sciencesTherapeutic approach0302 clinical medicinemicroRNAmedicineGene silencinglcsh:Neurosciences. Biological psychiatry. NeuropsychiatrymicroRNAhypoxiaGeneral NeuroscienceHypoxia (medical)medicine.disease030104 developmental biologymedicine.anatomical_structureyoganeuroprotectionmedicine.symptomNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Neuroscience
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An Assay to Determine Mechanisms of Rapid Autoantibody-Induced Neurotransmitter Receptor Endocytosis and Vesicular Trafficking in Autoimmune Encephal…

2019

N-Methyl-D-aspartate (NMDA) receptors (NMDARs) are among the most important excitatory neurotransmitter receptors in the human brain. Autoantibodies to the human NMDAR cause the most frequent form of autoimmune encephalitis involving autoantibody-mediated receptor cross-linking and subsequent internalization of the antibody-receptor complex. This has been deemed to represent the predominant antibody effector mechanism depleting the NMDAR from the synaptic and extra-synaptic neuronal cell membrane. To assess in detail the molecular mechanisms of autoantibody-induced NMDAR endocytosis, vesicular trafficking, and exocytosis we transiently co-expressed rat GluN1-1a-EGFP and GluN2B-ECFP alone or…

0301 basic medicineEndosomeautoantibodiesmedia_common.quotation_subjectN-Methyl-D-aspartate receptorsEndocytosisExocytosislcsh:RC346-42903 medical and health sciences0302 clinical medicineNeurotransmitter receptorendocytosisInternalizationReceptorlcsh:Neurology. Diseases of the nervous systemmedia_commonOriginal ResearchChemistryAutoantibodyautoimmune encephalitisCell biology030104 developmental biologynervous systemNeurologyRabNeurology (clinical)exocytosisvesicular trafficking030217 neurology & neurosurgerycross-linkingFrontiers in neurology
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Novel Insights of Effects of Pregabalin on Neural Mechanisms of Intracortical Disinhibition in Physiopathology of Fibromyalgia: An Explanatory, Rando…

2018

Submitted by DSpace Unilasalle (dspace@unilasalle.edu.br) on 2021-09-14T16:51:25Z No. of bitstreams: 1 adeitos.etal.pdf: 2278622 bytes, checksum: dd96bf75fdbab601238c2831da009c73 (MD5) Made available in DSpace on 2021-09-14T16:51:25Z (GMT). No. of bitstreams: 1 adeitos.etal.pdf: 2278622 bytes, checksum: dd96bf75fdbab601238c2831da009c73 (MD5) Previous issue date: 2018 Background: The fibromyalgia (FM) physiopathology involves an intracortical excitability/inhibition imbalance as measured by transcranial magnetic stimulation measures (TMS). TMS measures provide an index that can help to understand how the basal neuronal plasticity state (i.e., levels of the serum neurotrophins brain-derived n…

0301 basic medicineFibromyalgiashort intracortical inhibitionmedicine.medical_treatmentPregabalincortical silent periodPlaceboS100Blcsh:RC321-57103 medical and health sciencesBehavioral Neuroscience0302 clinical medicineFibromyalgiaNeuroplasticityMedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryBiological PsychiatryPregabalinaCortical silent periodbusiness.industryFator neurotrófico derivado do encéfaloFibromialgiaProteínas S100medicine.diseaseClinical TrialCrossover studyTranscranial magnetic stimulationPsychiatry and Mental healthBDNF030104 developmental biologyNeuropsychology and Physiological PsychologyNeurologyShort intracortical inhibitionDisinhibitionAnesthesiafibromyalgiaSilent periodmedicine.symptombusiness030217 neurology & neurosurgeryNeurosciencemedicine.drugFrontiers in Human Neuroscience
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Taurine as an Essential Neuromodulator during Perinatal Cortical Development

2017

A variety of experimental studies demonstrated that neurotransmitters are an important factor for the development of the central nervous system, affecting neurodevelopmental events like neurogenesis, neuronal migration, programmed cell death, and differentiation. While the role of the classical neurotransmitters glutamate and gamma-aminobutyric acid (GABA) on neuronal development is well established, the aminosulfonic acid taurine has also been considered as possible neuromodulator during early neuronal development. The purpose of the present review article is to summarize the properties of taurine as neuromodulator in detail, focusing on the direct involvement of taurine on various neurode…

0301 basic medicineGABA receptorsTaurineCentral nervous systemReviewBiologymigrationlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineCajal–Retzius cellsmedicinePremovement neuronal activityGlycine receptorlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeocortexGABAA receptorglycine receptorsNeurogenesisGlutamate receptorrodent030104 developmental biologymedicine.anatomical_structurechemistrynervous systemsubplatecerebral cortexNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Coexpresión de NG2/GFAP tras la diferenciación en células transfectadas con las mutaciones de GFAP y en células procedentes de gliomas indiferenciados

2020

Resumen: Introducción: La enfermedad de Alexander es una enfermedad rara causada por mutaciones en el gen que codifica la proteína glial ácida fibrilar (GFAP). En un estudio previo hemos observado que la diferenciación de neuroesferas transfectadas con estas mutaciones genera un tipo celular que comparte la expresión de GFAP y NG2. Objetivos: Determinar el efecto de las mutaciones en marcadores moleculares en comparación con células de glioma diferenciados que expresan simultáneamente GFAP y NG2. Métodos: Se utilizaron muestras de glioblastoma humana (GLM) y neuroesferas procedentes de rata transfectadas con mutaciones de GFAP para el análisis de la expresión tras diferenciación de GFAP y N…

0301 basic medicineGFAPmacromolecular substancesGliomalcsh:RC346-42903 medical and health sciences030104 developmental biology0302 clinical medicinenervous systemCaspase-3Alexander diseaseNG2Neurology (clinical)030217 neurology & neurosurgerylcsh:Neurology. Diseases of the nervous systemNeurología
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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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Improvements to Healthspan Through Environmental Enrichment and Lifestyle Interventions: Where Are We Now?

2020

Environmental enrichment (EE) is an experimental paradigm that is used to explore how a complex, stimulating environment can impact overall health. In laboratory animal experiments, EE housing conditions typically include larger-than-standard cages, abundant bedding, running wheels, mazes, toys, and shelters which are rearranged regularly to further increase stimulation. EE has been shown to improve multiple aspects of health, including but not limited to metabolism, learning and cognition, anxiety and depression, and immunocompetence. Recent advances in lifespan have led some researchers to consider aging as a risk factor for disease. As such, there is a pressing need to understand the pro…

0301 basic medicineGerontologymedia_common.quotation_subjectContext (language use)ReviewDiseasehealthspanlcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineQuality (business)hypothalamuslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymedia_commonEnvironmental enrichmentHPA axisGeneral NeuroscienceLongevityCognitionMedical research030104 developmental biologyBDNFhealthy agingenvironmental enrichmentAnxietymedicine.symptomPsychologylifespan030217 neurology & neurosurgeryNeuroscienceFrontiers in Neuroscience
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Oxidative Stress-Induced Axon Fragmentation Is a Consequence of Reduced Axonal Transport in Hereditary Spastic Paraplegia SPAST Patient Neurons

2020

Hereditary spastic paraplegia (HSP) is a group of inherited disorders characterized by progressive spasticity and paralysis of the lower limbs. Autosomal dominant mutations in SPAST gene account for ∼40% of adult-onset patients. We have previously shown that SPAST patient cells have reduced organelle transport and are therefore more sensitive to oxidative stress. To test whether these effects are present in neuronal cells, we first generated 11 induced pluripotent stem (iPS) cell lines from fibroblasts of three healthy controls and three HSP patients with different SPAST mutations. These cells were differentiated into FOXG1-positive forebrain neurons and then evaluated for multiple aspects …

0301 basic medicineHereditary spastic paraplegiaOxidative phosphorylationSpastinmedicine.disease_causelcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASTAxonFragmentation (cell biology)hereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGeneral Neuroscienceperoxisomesaxon transportmedicine.diseaseepothilone Daxon degenerationCell biology030104 developmental biologymedicine.anatomical_structurenervous systemForebrainAxoplasmic transport030217 neurology & neurosurgeryOxidative stressFrontiers in Neuroscience
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Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
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Shank3 Mice Carrying the Human Q321R Mutation Display Enhanced Self-Grooming, Abnormal Electroencephalogram Patterns, and Suppressed Neuronal Excitab…

2019

Shank3, a postsynaptic scaffolding protein involved in regulating excitatory synapse assembly and function, has been implicated in several brain disorders, including autism spectrum disorders (ASD), Phelan-McDermid syndrome, schizophrenia, intellectual disability, and mania. Here we generated and characterized a Shank3 knock-in mouse line carrying the Q321R mutation (Shank3Q321R mice) identified in a human individual with ASD that affects the ankyrin repeat region (ARR) domain of the Shank3 protein. Homozygous Shank3Q321R/Q321R mice show a selective decrease in the level of Shank3a, an ARR-containing protein variant, but not other variants. CA1 pyramidal neurons in the Shank3Q321R/Q321R hip…

0301 basic medicineHippocampusautism spectrum disorderBiologyNeurotransmissionElectroencephalographyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceExcitatory synapse assembly0302 clinical medicinePostsynaptic potentialexcitabilitymedicineself-groomingEEGMolecular Biologylcsh:Neurosciences. Biological psychiatry. Neuropsychiatrypatient mutationsOriginal Researchmedicine.diagnostic_testanxiety-like behaviorseizure susceptibilitymedicine.disease030104 developmental biologyShank3SchizophreniaExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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