Search results for "Friedreich’s ataxia"

showing 7 items of 7 documents

Reversible Axonal Dystrophy by Calcium Modulation in Frataxin-Deficient Sensory Neurons of YG8R Mice

2017

15 Pages, 8 Figures. The Supplementary Material for this article can be found online at: http://journal.frontiersin.org/article/10.3389/fnmol.2017.00264/full#supplementary-material

0301 basic medicineAtaxiaNeuriteFriedreich’s ataxiarare diseaseMitochondrionlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBAPTAmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyOriginal ResearchcalciumbiologyNeurodegenerationneurodegenerationFriedreich's ataxiaaxonal spheroidsmedicine.disease3. Good healthmitochondria030104 developmental biologyPeripheral neuropathychemistrynervous systemFrataxinbiology.proteinAxoplasmic transportmedicine.symptomNeuroscience030217 neurology & neurosurgeryNeuroscience
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Oxidative Stress, a Crossroad Between Rare Diseases and Neurodegeneration

2020

Oxidative stress is an imbalance between production and accumulation of oxygen reactive species and/or reactive nitrogen species in cells and tissues, and the capacity of detoxifying these products, using enzymatic and non-enzymatic components, such as glutathione. Oxidative stress plays roles in several pathological processes in the nervous system, such as neurotoxicity, neuroinflammation, ischemic stroke, and neurodegeneration. The concepts of oxidative stress and rare diseases were formulated in the eighties, and since then, the link between them has not stopped growing. The present review aims to expand knowledge in the pathological processes associated with oxidative stress underlying …

0301 basic medicineAtaxiaUnverricht–Lundborg disease (ULD)PhysiologyNeurodegeneration with brain iron accumulationClinical BiochemistryFriedreich’s ataxiaReviewmedicine.disease_causeBioinformaticsBiochemistry03 medical and health scienceschemistry.chemical_compoundLafora disease (LD)0302 clinical medicineMedicineprogressive myoclonus epilepsy (PME)Molecular BiologyNeuroinflammationReactive nitrogen speciesneurodegenerative disorders with brain iron accumulation (NBIA)business.industryNeurodegenerationlcsh:RM1-950NeurotoxicityCell Biologymedicine.diseaseDravet syndromeCharcot-Marie-Tooth disease (CMT)030104 developmental biologylcsh:Therapeutics. Pharmacologychemistrymedicine.symptombusinessMyoclonusinherited retinal dystrophy (IRD)030217 neurology & neurosurgeryOxidative stressAntioxidants
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The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.

2019

Friedreich’s ataxia (FRDA) is a rare early-onset degenerative disease that affects both the central and peripheral nervous systems, and other extraneural tissues, mainly the heart and endocrine pancreas. This disorder progresses as a mixed sensory and cerebellar ataxia, primarily disturbing the proprioceptive pathways in the spinal cord, peripheral nerves and nuclei of the cerebellum. FRDA is an inherited disease with an autosomal recessive pattern caused by an insufficient amount of the nuclear-encoded mitochondrial protein frataxin, which is an essential and highly evolutionary conserved protein whose deficit results in iron metabolism dysregulation and mitochondrial dysfunction. The firs…

0301 basic medicineCerebellumAtaxiaFriedreich’s ataxiaReviewMitochondrionmedicine.disease_causelcsh:RC321-57103 medical and health sciencesiron0302 clinical medicineDegenerative diseasemedicineoxidative stresslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationReactive oxygen speciesfrataxinbiologyCerebellar ataxialipid deregulationGeneral Neurosciencemedicine.diseaseanimal modelsCell biology030104 developmental biologymedicine.anatomical_structurechemistryFrataxinbiology.proteiniron chelatorsmedicine.symptom030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in neuroscience
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Thioredoxin and Glutaredoxin Systems as Potential Targets for the Development of New Treatments in Friedreich’s Ataxia

2020

The thioredoxin family consists of a small group of redox proteins present in all organisms and composed of thioredoxins (TRXs), glutaredoxins (GLRXs) and peroxiredoxins (PRDXs) which are found in the extracellular fluid, the cytoplasm, the mitochondria and in the nucleus with functions that include antioxidation, signaling and transcriptional control, among others. The importance of thioredoxin family proteins in neurodegenerative diseases is gaining relevance because some of these proteins have demonstrated an important role in the central nervous system by mediating neuroprotection against oxidative stress, contributing to mitochondrial function and regulating gene expression. Specifical…

0301 basic medicinePhysiologyClinical BiochemistryFriedreich’s ataxiaContext (language use)ReviewMitochondrionBiologyBiochemistrythioredoxins03 medical and health sciences0302 clinical medicineGlutaredoxinGene expressionTranscriptional regulationoxidative stressMolecular BiologyGeneglutaredoxinslcsh:RM1-950Cell BiologyCell biologylcsh:Therapeutics. Pharmacology030104 developmental biologyThioredoxin030217 neurology & neurosurgeryFunction (biology)Antioxidants
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Impact of

2018

Drosophila melanogaster has been for over a century the model of choice of several neurobiologists to decipher the formation and development of the nervous system as well as to mirror the pathophysiological conditions of many human neurodegenerative diseases. The rare disease Friedreich’s ataxia (FRDA) is not an exception. Since the isolation of the responsible gene more than two decades ago, the analysis of the fly orthologue has proven to be an excellent avenue to understand the development and progression of the disease, to unravel pivotal mechanisms underpinning the pathology and to identify genes and molecules that might well be either disease biomarkers or promising targets for therap…

frataxinDrug Evaluation PreclinicalFriedreich’s ataxiaReviewLipid Metabolismdrug screensDisease Models AnimalOxidative Stressendoplasmic reticulumDrosophila melanogasterPhenotypeironFriedreich AtaxiaIron-Binding Proteinsmetal homeostasisAnimalsHumansGenetic Predisposition to DiseaseGene Silencinggenetic screensInternational journal of molecular sciences
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Antioxidant Therapies and Oxidative Stress in Friedreich´s Ataxia: The Right Path or Just a Diversion?

2020

Friedreich's ataxia is the commonest autosomal recessive ataxia among population of European descent. Despite the huge advances performed in the last decades, a cure still remains elusive. One of the most studied hallmarks of the disease is the increased production of oxidative stress markers in patients and models. This feature has been the motivation to develop treatments that aim to counteract such boost of free radicals and to enhance the production of antioxidant defenses. In this work, we present and critically review those 'antioxidant' drugs that went beyond the disease's models and were approved for its application in clinical trials. The evaluation of these trials highlights some …

reactive oxygen speciesFriedreich’s ataxia; clinical trials; oxidative stress; antioxidant therapies; reactive oxygenspecies; scavengers; antioxidant response; mitochondrial metabolism; ferroptosisclinical trialsmitochondrial metabolismantioxidant responseEstrès oxidatiulcsh:RM1-950Friedreich’s ataxiaReviewFriedreich´s ataxia590 Tiere (Zoologie)Antioxidantsferroptosisscavengerslcsh:Therapeutics. Pharmacology570 Biowissenschaften Biologieddc:590oxidative stressantioxidant therapiesddc:570Antioxidants
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