Search results for "NEURODEGENERATION"

showing 10 items of 268 documents

Yunis-Varón Syndrome Is Caused by Mutations in FIG4, Encoding a Phosphoinositide Phosphatase

2013

Yunis-Varón syndrome (YVS) is an autosomal-recessive disorder with cleidocranial dysplasia, digital anomalies, and severe neurological involvement. Enlarged vacuoles are found in neurons, muscle, and cartilage. By whole-exome sequencing, we identified frameshift and missense mutations of FIG4 in affected individuals from three unrelated families. FIG4 encodes a phosphoinositide phosphatase required for regulation of PI(3,5)P(2) levels, and thus endosomal trafficking and autophagy. In a functional assay, both missense substitutions failed to correct the vacuolar phenotype of Fig4-null mouse fibroblasts. Homozygous Fig4-null mice exhibit features of YVS, including neurodegeneration and enlarg…

GenotypePhosphataseMicrognathismMolecular Sequence DataLimb Deformities CongenitalMutation MissenseBiologyCompound heterozygositymedicine.disease_causeFrameshift mutation03 medical and health sciencesMice0302 clinical medicinePhosphatidylinositol PhosphatesEctodermal DysplasiaReportmedicineGeneticsMissense mutationAnimalsHumansExomeGenetic Predisposition to DiseaseGenetics(clinical)Yunis–Varon syndromeFrameshift MutationGenetics (clinical)030304 developmental biology0303 health sciencesMutationBone DevelopmentBase SequenceFlavoproteinsNeurodegenerationSequence Analysis DNAFibroblastsmedicine.diseaseMolecular biologyPhenotypePhosphoric Monoester HydrolasesCleidocranial Dysplasia030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Deletion of myosin VI causes slow retinal optic neuropathy and age-related macular degeneration (AMD)-relevant retinal phenotype

2015

The unconventional myosin VI, a member of the actin-based motor protein family of myosins, is expressed in the retina. Its deletion was previously shown to reduce amplitudes of the a- and b-waves of the electroretinogram. Analyzing wild-type and myosin VI-deficient Snell’s Waltzer mice in more detail, the expression pattern of myosin VI in retinal pigment epithelium, outer limiting membrane, and outer plexiform layer could be linked with differential progressing ocular deficits. These encompassed reduced a-waves and b-waves and disturbed oscillatory potentials in the electroretinogram, photoreceptor cell death, retinal microglia infiltration, and formation of basal laminar deposits. A pheno…

Genotypegenetic structuresOuter retinaTranslocator protein TSPOOuter plexiform layermacromolecular substancesBiologyRetinaPhotoreceptor cellMouse modelStereociliaMacular DegenerationMiceCellular and Molecular Neurosciencechemistry.chemical_compoundOptic Nerve DiseasesMyosinmedicineAnimalsBipolar cellMolecular BiologyPharmacologyRetinaRetinal pigment epitheliumMyosin Heavy ChainsNeurodegenerationInner retinaChoriocapillarisRetinalCell BiologyAnatomyMacular degenerationmedicine.diseaseSynapseeye diseasesCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryMolecular MedicineMicrogliasense organsGene DeletionResearch ArticlePhotoreceptor Cells VertebrateCellular and Molecular Life Sciences
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Neuroprotective potential of Ginkgo biloba in retinal diseases

2019

AbstractLike other tissues of the central nervous system, the retina is susceptible to damage by oxidative processes that result in several neurodegenerative disease such as age-related macular degeneration, diabetic retinopathy, glaucoma, ischaemic retinal disease, retinal disease produced by light oxidation, and detached retina, among other diseases. The use of antioxidant substances is a solution to some health problems caused by oxidative stress, because they regulate redox homeostasis and reduce oxidative stress. This is important for neurodegeneration linked to oxidation processes. In line with this, Ginkgo biloba is a medicinal plant with excellent antioxidant properties whose effect…

Ginkgo biloba - Uso terapéutico.Pharmaceutical SciencePharmacologymedicine.disease_cause01 natural sciencesNeuroprotectionAnalytical Chemistrychemistry.chemical_compoundRetinal DiseasesGinkgo biloba - Therapeutic use.Drug DiscoveryAnimalsHumansMedicinePharmacologyRetinabiologyPlant Extracts010405 organic chemistrybusiness.industryGinkgo bilobaRetina - Diseases - Treatment.System nervous - Degeneration - Treatment.Organic ChemistryNeurodegenerationGinkgo bilobaNeurodegenerative DiseasesRetinalDiabetic retinopathyMacular degenerationmedicine.diseasebiology.organism_classificationEye - Diseases - Treatment.0104 chemical sciencesSistema nervioso - Degeneración - Tratamiento.010404 medicinal & biomolecular chemistryNeuroprotective Agentsmedicine.anatomical_structureComplementary and alternative medicinechemistryOjos - Enfermedades - Tratamiento.Molecular MedicinebusinessOxidative stressPhytotherapyRetina - Enfermedades - Tratamiento.
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Protective role of heat shock proteins in Parkinson's disease.

2010

Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease. Despite a large amount of research, the pathogenetic mechanism of these diseases has not yet been clarified. Abnormal protein folding, oxidative stress, mitochondrial dysfunction, and apoptotic mechanisms have all been reported as causes of neurodegenerative diseases in association with neuroinflammatory mechanisms which, by generating deleterious molecules, could promote the cascade of events leading to neurodegeneration. Heat shock proteins (HSPs) play a central role in preventing protein misfolding and inhibiting apoptotic activity, and represent a class of proteins potentially involve…

Heat shock proteins Parkinson disease neuroprotective roleParkinson's diseasebiologyNeurodegenerationParkinson DiseaseDiseasemedicine.diseasemedicine.disease_causeHsp90Hsp70PathogenesisNeurologyHeat shock proteinImmunologymedicinebiology.proteinAnimalsHumansHSP70 Heat-Shock ProteinsNeurology (clinical)HSP90 Heat-Shock ProteinsNeuroscienceOxidative stressHeat-Shock ProteinsNeuro-degenerative diseases
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AAV Vector–mediated RNAi of Mutant Huntingtin Expression Is Neuroprotective in a Novel Genetic Rat Model of Huntington's Disease

2008

We report the characterization of a new rapid-onset model of Huntington's disease (HD) generated by adeno-associated virus (AAV) vector–mediated gene transfer of N-terminal huntingtin (htt) constructs into the rat striatum. Expression of exon 1 of mutant htt containing 70 CAG repeats rapidly led to neuropathological features associated with HD. In addition, we report novel data relating to neuronal transduction of AAV vectors that modulated the phenotype observed in this model. Quantitative reverse transcriptase–polymerase chain reaction (RT–PCR) revealed that AAV vector–mediated expression in the striatum increased by >100-fold as compared to the endogenous htt level. Moreover, AAV vectors…

HuntingtinvirusesGenetic VectorsNerve Tissue ProteinsSubstantia nigraBiologyArticleViral vectorHuntington's diseaseRNA interferenceDrug DiscoverymedicineHuntingtin ProteinGeneticsAnimalsHumansMolecular BiologyNeuronsPharmacologyHuntingtin ProteinGene knockdownReverse Transcriptase Polymerase Chain ReactionNeurodegenerationNuclear ProteinsExonsGenetic TherapyDependovirusmedicine.diseaseMolecular biologyCorpus StriatumRatsHuntington DiseaseNeuroprotective AgentsPhenotypenervous systemMolecular MedicineRNA InterferenceMolecular Therapy
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Guanosine Protects Glial Cells Against 6-Hydroxydopamine Toxicity

2014

Increasing body of evidence indicates that neuron-neuroglia interaction may play a key role in determining the progression of neurodegenerative diseases including Parkinson’s disease (PD), a chronic pathological condition characterized by selective loss of dopaminergic (DA) neurons in the substantia nigra. We have previously reported that guanosine (GUO) antagonizes MPP+-induced cytotoxicity in neuroblastoma cells and exerts neuroprotective effects against 6-hydroxydopamine (6-OHDA) and beta-amyloid-induced apoptosis of SH-SY5Y cells. In the present study we demonstrate that GUO protected C6 glioma cells, taken as a model system for astrocytes, from 6-OHDA-induced neurotoxicity. We show tha…

HydroxydopaminebiologyChemistryNeurodegenerationNeurotoxicitySubstantia nigraNucleoside transporterPharmacologymedicine.diseaseNeuroprotectionNeurotrophic factorsbiology.proteinmedicinePI3K/AKT/mTOR pathway
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Contribution of Extracellular Vesicles and Molecular Chaperones in Age-Related Neurodegenerative Disorders of the CNS

2023

Many neurodegenerative disorders are characterized by the abnormal aggregation of misfolded proteins that form amyloid deposits which possess prion-like behavior such as self-replication, intercellular transmission, and consequent induction of native forms of the same protein in surrounding cells. The distribution of the accumulated proteins and their correlated toxicity seem to be involved in the progression of nervous system degeneration. Molecular chaperones are known to maintain proteostasis, contribute to protein refolding to protect their function, and eliminate fatally misfolded proteins, prohibiting harmful effects. However, chaperone network efficiency declines during aging, prompt…

Inorganic ChemistryOrganic ChemistryGeneral MedicinePhysical and Theoretical Chemistrycentral nervous system extracellular vesicles chaperones system aging neurodegenerationMolecular BiologySpectroscopyCatalysisComputer Science Applications
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Phenothiazines interfere with dopaminergic neurodegeneration in Caenorhabditis elegans models of Parkinson's disease

2010

Oxidative stress is involved in the pathogenesis of various neurodegenerative disorders, conventional antioxidant strategies have yet been of limited success. We have employed transgenic Caenorhabditis elegans expressing DsRed2 in dopaminergic neurons and CFP pan-neuronally, to characterize in larval and adult animals the effects of rotenone and 1-methyl-4-phenyl-pyridinium (MPP(+)) on the dopaminergic system. Investigating the antioxidant phenothiazine and different derived antipsychotic drugs, it was found that free phenothiazine exerted strong neuroprotection at the cellular level and resulted in a better performance in behavioral assays, whereas apomorphine and other dopamine agonists o…

InsecticidesApomorphineChlorpromazineDopamineBiologyPharmacologyNeuroprotectionlcsh:RC321-571Animals Genetically Modifiedchemistry.chemical_compoundAntipsychotic drugParkinsonian DisordersDopaminePhenothiazinesRotenonemedicineAnimalsHumansChlorpromazineCaenorhabditis eleganslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationNeuronsDopaminergic neuronModels GeneticNeurodegenerationDopaminergicRotenonemedicine.diseaseDisease Models AnimalNeuroprotective AgentsNeurologychemistryDopamine receptorNerve DegenerationAntioxidantTricyclicmedicine.drugAntipsychotic AgentsNeurobiology of Disease
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miRNAs and Genes Involved in the Interplay between Ocular Hypertension and Primary Open-Angle Glaucoma. Oxidative Stress, Inflammation, and Apoptosis…

2021

Este artículo se encuentra disponible en la siguiente URL: https://www.mdpi.com/2077-0383/10/11/2227 En esta investigación también participan: Mar Valero Vello, Silvia M. Sanz González, José E. O'Connor, David Galarreta Mira, María D. Pinazo-Durán y Vicente Zanón Moreno. Este artículo pertenece al número especial "Recent Clinical Research on Glaucoma". Glaucoma has no cure and is a sight-threatening neurodegenerative disease affecting more than 100 million people worldwide, with primary open angle glaucoma (POAG) being the most globally prevalent glaucoma clinical type. Regulation of gene expression and gene networks, and its multifactorial pathways involved in glaucoma disease are landmark…

Intraocular pressureBiochemical markers.Open angle glaucomagenetic structuresGlaucomaOcular hypertensionDiseaseBioinformaticsArticle03 medical and health sciences0302 clinical medicineGene expressionmicroRNAApoptosis.Medicineoxidative stressGlaucoma.genes030304 developmental biologyRegulation of gene expressionEstrés oxidativo.next generation sequencing0303 health sciencesbusiness.industryPresión intraocular.apoptosisneurodegenerationIntraocular pressure.RMarcadores bioquímicos.tearsbiomarkersGeneral Medicinemedicine.diseasesignaling pathwayseye diseasesOxidative stress.glaucomainflammationmiRNAs030221 ophthalmology & optometryocular hypertensionMedicinebusinessJournal of Clinical Medicine
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Measuring network disruption in neurodegenerative diseases: New approaches using signal analysis

2019

Advanced neuroimaging has increased understanding of the pathogenesis and spread of disease, and offered new therapeutic targets. MRI and positron emission tomography have shown that neurodegenerative diseases including Alzheimer’s disease (AD), Lewy body dementia (LBD), Parkinson’s disease (PD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) are associated with changes in brain networks. However, the underlying neurophysiological pathways driving pathological processes are poorly defined. The gap between what imaging can discern and underlying pathophysiology can now be addressed by advanced techniques that explore the cortical neural synchro…

Lewy Body Diseasemedicine.medical_treatmentElectroencephalographysurgery03 medical and health sciences0302 clinical medicineNeuroimagingAlzheimer DiseasemedicineDementiaHumans1506Amyotrophic lateral sclerosisNeurodegeneration030304 developmental biologyneurology (clinical)0303 health sciencesLewy bodymedicine.diagnostic_testbusiness.industryAmyotrophic Lateral Sclerosissurgery; neurology (clinical); psychiatry and mental healthMagnetoencephalographyElectroencephalographyNeurodegenerative DiseasesParkinson DiseaseMagnetoencephalographymedicine.diseaseTranscranial Magnetic Stimulation3. Good healthTranscranial magnetic stimulationpsychiatry and mental healthFrontotemporal DementiaNerve NetbusinessNeuroscience030217 neurology & neurosurgeryFrontotemporal dementiaJournal of Neurology, Neurosurgery, and Psychiatry
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