Search results for "Charcot"

showing 10 items of 39 documents

The gene encoding ganglioside-induced differentiation-associated protein 1 is mutated in axonal Charcot-Marie-Tooth type 4A disease

2001

We identified three distinct mutations and six mutant alleles in GDAP1 in three families with axonal Charcot-Marie-Tooth (CMT) neuropathy and vocal cord paresis, which were previously linked to the CMT4A locus on chromosome 8q21.1. These results establish the molecular etiology of CMT4A (MIM 214400) and suggest that it may be associated with both axonal and demyelinating phenotypes.

Malecongenital hereditary and neonatal diseases and abnormalitiesDNA Mutational AnalysisMolecular Sequence DataMutantMutation MissenseNeural ConductionGenes RecessiveNerve Tissue ProteinsLocus (genetics)BiologyPolymerase Chain ReactionFrameshift mutationCharcot-Marie-Tooth DiseaseGeneticsHumansMissense mutationAge of OnsetAlleleChildFrameshift MutationGeneAllelesGeneticsBrainInfantExonsAnatomyPhenotypeAxonsPedigreeAmino Acid SubstitutionHaplotypesSpinal CordCodon NonsenseSpainChild PreschoolFemaleLod ScoreVocal cord paresisChromosomes Human Pair 8Demyelinating DiseasesNature Genetics
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Patient-reported impact of Charcot-Marie-Tooth disease: protocol for a real-world digital lifestyle study

2021

Abstract Background Charcot-Marie-Tooth disease (CMT) is a rare, chronic, progressive motor and sensory neuropathy that affects the peripheral nervous system, leading to progressive, predominantly distal muscle weakness, atrophy, sensory loss and progressive limb dysfunction. As with many rare diseases, there is a lack of patient-reported data with which to understand and address patient needs. This study aims to explore the real-world impact of CMT from the patient perspective. Methods This is a prospective, digital lifestyle study of at least 2,000 people with CMT, >18 years, resident in the following countries: France, Germany, Italy, Spain, the UK and the USA. Participants will be re…

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyDemographicsDiseaseUnmet needs03 medical and health sciencesTooth disease0302 clinical medicinePhysical medicine and rehabilitationCharcot-Marie-Tooth DiseaseMedicineHumans030212 general & internal medicineobservationalPatient Reported Outcome MeasuresProspective StudiesLife StyleSelection (genetic algorithm)Protocol (science)business.industryIdentifierpatient-reported outcomesinternationalburden of illnessObservational studyFemaleNeurology (clinical)business030217 neurology & neurosurgery
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Pigment variant of neuronal ceroid-lipofuscinosis

1995

A 6-year-old girl had progressive ataxia, and visual disturbances resulting in blindness. She died in her sleep at age 22 years. She shared with her sister and paternal relatives bilateral pes cavus deformities and impaired deep-tendon reflexes which suggested Charcot-Marie-Tooth disease. Her sister, who also had both polyneuropathy and a progressive central nervous system (CNS) disease, did not have pigmentary retinopathy. At autopsy, the patient was found to have neuronal ceroid-lipofuscinosis (NCL) marked by intraneuronal accumulation of autofluorescent granular lipopigments in ballooned perikarya and conspicuous extraneuronal pigmentation of subcortical grey matter, but without axonal s…

Malemedicine.medical_specialtyPathologyPostmortem studiesNeurologyCentral nervous systemAutopsyBiologyGrey matterEpitheliumNuclear FamilyDiagnosis DifferentialCharcot-Marie-Tooth DiseaseNeuronal Ceroid-LipofuscinosesmedicineNeuropilHumansChildGenetics (clinical)Cerebral CortexNeuronsPigmentationPigments BiologicalAnatomymedicine.diseaseMicroscopy ElectronKidney Tubulesmedicine.anatomical_structureSpinal CordFemaleNeuronal ceroid lipofuscinosisPolyneuropathyAmerican Journal of Medical Genetics
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Metabolic and Functional Improvements in a Patient with Charcot-Marie-Tooth Disease Type 2 after EGCG Administration: A Case Report.

2021

Background and objectives: The aim of this study was to report a case of a patient with Charcot-Marie-Tooth disease type 2 (CMT2) treated with epigallocatechin gallate (EGCG) for 4 months in order to assess its therapeutic potential in CMT2. Materials and Methods: The study included a brother and a sister who have CMT2. The sister received 800 mg of EGCG for 4 months, while her brother received placebo for the same period of time. Both participants were assessed before and after daily administration by means of anthropometry; analysis of inflammatory and oxidation markers of interleukin-6 (IL-6) and paraoxonase 1 (PON1) in the blood sample; and motor tests: 2-min walk test (2MWT), 10-m walk…

Malemedicine.medical_specialtyepigallocatechin gallateCase ReportWalk TestDiseaseEpigallocatechin gallatePlaceboCatechinchemistry.chemical_compoundTooth diseaseCharcot-Marie-Tooth DiseaseInternal medicineMedicineHumansCharcot-Marie-Tooth disease type 2lcsh:R5-920IL-6biologyHand Strengthbusiness.industrymotor activityAryldialkylphosphataseParaoxonaseparaoxonase 1General MedicineAnthropometryPON1chemistryWalk testbiology.proteinFemalebusinesslcsh:Medicine (General)
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Lack of GDAP1 induces neuronal calcium and mitochondrial defects in a knockout mouse model of Charcot-Marie-tooth neuropathy

2015

27 páginas, 9 figuras.

Mitochondrial proteinCancer Researchlcsh:QH426-470Nerve Tissue ProteinsBiologyMitochondrionCharcot-Marie-Tooth diseaseGDAP1 geneMiceGeneticsAutophagyAnimalsCalcium SignalingMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsCytoskeletonCalcium signalingGeneticsVoltage-dependent calcium channelEndoplasmic reticulumAutophagyBiología y Biomedicina / BiologíaAxonsCell biologyMitochondriaMitochondrialMice Inbred C57BLAlpha tubulinlcsh:Geneticsmitochondrial fusionKnockout mouseMitochondrial fissionCalcium ChannelsAnimal cellGene DeletionResearch Article
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Mitochondrial defects and neuromuscular degeneration caused by altered expression of Drosophila Gdap1: implications for the Charcot–Marie–Tooth neuro…

2014

One of the genes involved in Charcot-Marie-Tooth (CMT) disease, an inherited peripheral neuropathy, is GDAP1. In this work, we show that there is a true ortholog of this gene in Drosophila, which we have named Gdap1. By up- and down-regulation of Gdap1 in a tissue-specific manner, we show that altering its levels of expression produces changes in mitochondrial size, morphology and distribution, and neuronal and muscular degeneration. Interestingly, muscular degeneration is tissue-autonomous and not dependent on innervation. Metabolic analyses of our experimental genotypes suggest that alterations in oxidative stress are not a primary cause of the neuromuscular degeneration but a long-term c…

Nerve Tissue ProteinsDiseaseDegeneration (medical)BiologyMitochondrionMitochondrial Sizemedicine.disease_causeRetinaCharcot-Marie-Tooth DiseaseGeneticsmedicineAnimalsDrosophila ProteinsHumansMolecular BiologyGenePhylogenyGenetics (clinical)F-Box ProteinsNeurodegenerationNeuromuscular DiseasesGeneral MedicineAnatomymedicine.diseaseMitochondriaCell biologyTissue DegenerationDisease Models AnimalDrosophila melanogasterGene Expression RegulationMitochondrial SizeOxidative stressHuman Molecular Genetics
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Junctophilin-1 is a modifier gene of GDAP1-related Charcot-Marie-Tooth disease.

2014

Mutations in the GDAP1 gene cause different forms of Charcot-Marie-Tooth (CMT) disease, and the primary clinical expression of this disease is markedly variable in the dominant inheritance form (CMT type 2K; CMT2K), in which carriers of the GDAP1 p.R120W mutation can display a wide range of clinical severity. We investigated the JPH1 gene as a genetic modifier of clinical expression variability because junctophilin-1 (JPH1) is a good positional and functional candidate. We demonstrated that the JPH1-GDAP1 cluster forms a paralogon and is conserved in vertebrates. Moreover, both proteins play a role in Ca(2+) homeostasis, and we demonstrated that JPH1 is able to restore the store-operated Ca…

Nerve Tissue ProteinsDiseaseMitochondrionBiologyCell LineEvolution MolecularMiceCharcot-Marie-Tooth DiseaseGeneticsAnimalsHumansGenetic Predisposition to DiseaseStromal Interaction Molecule 1Molecular BiologyGeneGenetics (clinical)PhylogenyGenes ModifierActivator (genetics)Endoplasmic reticulumMembrane ProteinsSTIM1General MedicinePhenotypeMolecular biologyMitochondriaNeoplasm ProteinsMutationCalciumHomeostasisHuman molecular genetics
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Cell expression of GDAP1 in the nervous system and pathogenesis of Charcot-Marie-Tooth type 4A disease

2007

Abstract Mutations in the mitochondrial protein GDAP1 are the cause of Charcot-Marie-Tooth type 4A disease (CMT4A), a severe form of peripheral neuropathy associated with either demyelinating, axonal or intermediate pheno-types. GDAP1 is located in the outer mitochondrial membrane and it seems that may be related with the mitochondrial network dynamics. We are interested to define cell expression in the nervous system and the effect of mutations in mitochondrial morphology and pathogenesis of the disease. We investigated GDAP1 expression in the nervous system and dorsal root ganglia (DRG) neuron cultures. GDAP1 is expressed in motor and sensory neurons of the spinal cord and other large neu…

Nervous systemCMT4A mutations and pathogenesisPathologymedicine.medical_specialtyperipheral neuropathyCharcot-Marie-Tooth type 4A diseaseMutation MissenseGene ExpressionImages in Cellular / Molecular MedicineNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_causeNervous SystemPathogenesisMicePurkinje CellsCharcot-Marie-Tooth DiseaseInterneuronsGanglia SpinalChlorocebus aethiopsmedicineAnimalsHumansNeurons AfferentCells CulturedMotor NeuronsMutationfusion and fission pathwayPyramidal CellsCell Biologymedicine.diseaseSpinal cordImmunohistochemistrymitochondrial dynamicsCell biologyOlfactory bulbRatsmedicine.anatomical_structurePeripheral neuropathynervous systemAnimals NewbornSpinal CordCOS CellsMolecular MedicineNeuronHeLa CellsJournal of Cellular and Molecular Medicine
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Characterization of molecular mechanisms underlying the axonal Charcot–Marie–Tooth neuropathy caused by MORC2 mutations

2019

Mutations in MORC2 lead to an axonal form of Charcot-Marie-Tooth (CMT) neuropathy type 2Z. To date, 31 families have been described with mutations in MORC2, indicating that this gene is frequently involved in axonal CMT cases. While the genetic data clearly establish the causative role of MORC2 in CMT2Z, the impact of its mutations on neuronal biology and their phenotypic consequences in patients remains to be clarified. We show that the full-length form of MORC2 is highly expressed in both embryonic and adult human neural tissues and that Morc2 expression is dynamically regulated in both the developing and the maturing murine nervous system. To determine the effect of the most common MORC2…

Nervous systemSensory Receptor CellsCellBiologymedicine.disease_causeNeural Stem CellsCharcot-Marie-Tooth DiseaseGeneticsmedicineAnimalsHumansMolecular BiologyGeneEmbryonic Stem CellsGenetics (clinical)MutationGeneral MedicineFibroblastsPhenotypeEmbryonic stem cellAxonsNeural stem cellPathophysiologyRatsCell biologymedicine.anatomical_structureGene Expression Regulationnervous systemMutationTranscription FactorsHuman Molecular Genetics
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Fisiopatología mitocondrial en la neuropatía de Charcot-Marie-Tooth asociada al gen GDAP1

2020

Las mutaciones en el gen GDAP1, que codifica una proteína localizada en la membrana mitocondrial externa, causan la neuropatía hereditaria de Charcot-Marie-Tooth (CMT), caracterizada por una degeneración progresiva de los nervios periféricos motores y sensitivos. Hoy en día, todavía se desconocen los mecanismos celulares que desencadenan la disfunción neuronal en la enfermedad de CMT relacionada con la deficiencia de GDAP1. En este trabajo, hemos utilizado los cultivos primarios de motoneuronas de la médula espinal de ratones deficientes en GDAP1, para investigar el papel de esta proteína en la biología neuronal y dilucidar los mecanismos implicados en la fisiopatología de la enfermedad. Nu…

NeurodegeneraciónCharcot-Marie-ToothUNESCO::CIENCIAS MÉDICASGDAP1Mitocondria:CIENCIAS MÉDICAS [UNESCO]
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