Search results for "Trinucleotide repeat"

showing 10 items of 46 documents

GAA trinucleotide repeat expansion in variant Friedreich's ataxia families.

1997

Phenotypic variants in Friedreich's ataxia include late onset, preservation of the lower limbs tendon reflexes, and slow progression. We describe clinical and electrophysiological features from three families with Friedreichlike phenotypes. Friedreich's ataxia diagnosis was confirmed by finding two allelic expansions of the GAA trinucleotide repeat at the X25 gene. In family 1 both patients had a late-onset phenotype with preservation of knee and ankle jerks, lack of cardiomyopathy, and preserved H reflex. One of them did not have electrophysiologic evidence of sensory axonal neuropathy. Patients from family 2 showed variability in the age of onset, and 2 out of 3 affected children had hype…

AdultMaleReflex Stretchcongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtySensory axonal neuropathyAtaxiaPhysiologyGenetic LinkageAction PotentialsLate onsetBiologyH-ReflexCellular and Molecular NeuroscienceDegenerative diseaseTrinucleotide RepeatsPhysiology (medical)medicineHumansNeurons AfferentChildAllelesLegGenetic VariationDNACardiomyopathy Hypertrophicmedicine.diseasePedigreePeripheral neuropathyFriedreich AtaxiaReflexDisease ProgressionFemaleNeurology (clinical)medicine.symptomAge of onsetTrinucleotide repeat expansionMusclenerve
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Central motor conduction time by magnetic stimulation of the cortex and peripheral nerve conduction follow-up studies in Friedreich's ataxia.

1998

A follow-up clinical study, peripheral motor and sensory nerve conduction velocities and central motor conduction by magnetic stimulation of the cortex were performed in 13 patients with classical Friedreich's ataxia (FA) phenotype, for a period of 9-12 years. Clinical worsening was unrelated to peripheral nerve abnormalities. The amplitude of the nerve action potentials and delayed conduction velocity remained unchanged for several years. Central motor conduction times were abnormal in all patients. Clinical conditions worsened significantly between successive examinations with significant increments in threshold and significant decrement of the amplitude of motor evoked potentials. The re…

AdultMalemedicine.medical_specialtyAtaxiaAdolescentNeural ConductionMotor nerveElectromyographyNerve conduction velocityMagneticsSural NerveTrinucleotide RepeatsInternal medicineCerebellumPhysical StimulationReaction TimeMedicineHumansNeurons AfferentPeripheral NervesChildMuscle SkeletalNeural ConductionMotor Neuronsmedicine.diagnostic_testbusiness.industryElectromyographyGeneral NeurosciencePyramidal CellsMotor CortexMiddle AgedMedian Nervemedicine.anatomical_structureFriedreich AtaxiaPeripheral nervous systemCardiologyDisease ProgressionFemaleNeurology (clinical)medicine.symptomH-reflexbusinessNeuroscienceSensory nerveFollow-Up StudiesElectroencephalography and clinical neurophysiology
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Hypo-excitability of cortical areas in patients affected by Friedreich ataxia: A TMS study

2005

The aim of the study was to explore excitability of a motor and a non-motor (visual) area in patients affected by Friedreich ataxia and to correlate neurophysiological data with clinical parameters. Seven patients (3M/4F) and ten healthy controls (5M/5F) participated in the study. The hot-spot for activation of right abductor pollicis brevis was checked by means of a figure-of-eight coil and the motor threshold (MT) on this point was recorded. The phosphene threshold (PT) was measured by means of a focal coil over the occipital cortex as the lower intensity of magnetic stimulation able to induce the perception of phosphenes. The patients showed a significantly higher mean PT (p<.03) and MT …

AdultMalemedicine.medical_specialtyCerebellumAtaxiaAdolescentPhosphenesCentral nervous system diseaseMagneticsCortical excitability TMS Cerebellum Friedreich ataxia Visual cortex Motor cortex Hypo-excitabilityInternal medicineSensory thresholdCortex (anatomy)medicineHumansVisual CortexBrain MappingMotor Cortexmedicine.diseaseElectric StimulationSurgerymedicine.anatomical_structurePhospheneVisual cortexNeurologyFriedreich AtaxiaSensory ThresholdsCardiologyFemaleNeurology (clinical)medicine.symptomTrinucleotide Repeat ExpansionPsychologyMotor cortexJournal of the Neurological Sciences
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Phenotype Correlation and Intergenerational Dynamics of the Friedreich Ataxia GAA Trinucleotide Repeat

1997

Summary The Friedreich ataxia (FA) mutation has recently been identified as an unstable trinucleotide GAA repeat present 7–22 times in the normal population but amplified as many as > 1, 000 times in FA. Since it is an autosomal recessive disease, FA does not show typical features observed in other dynamic mutation disorders, such as genetic anticipation. We have analyzed the GAA repeat in 104 FA patients and 163 carrier relatives previously defined by linkage analysis. The GAA expansion was detected in all patients, most (94%) of them being ho-mozygous for the mutation. We have demonstrated that clinical variability in FA is related to the size of the expanded alleles: milder forms of the …

AtaxiaAdolescentGenetic LinkagePopulationBiologyTrinucleotide RepeatsMeiosisGenetic linkageGene duplicationGeneticsmedicineHumansGenetics(clinical)AlleleChildeducationGenetics (clinical)Geneticseducation.field_of_studyGene AmplificationPhenotypeFriedreich AtaxiaMutationMutation (genetic algorithm)Dynamic mutationmedicine.symptomResearch ArticleThe American Journal of Human Genetics
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Muscleblind isoforms are functionally distinct and regulate α-actinin splicing

2007

Drosophila Muscleblind (Mbl) proteins control terminal muscle and neural differentiation, but their molecular function has not been experimentally addressed. Such an analysis is relevant as the human Muscleblind-like homologs (MBNL1-3) are implicated in the pathogenesis of the inherited muscular developmental and degenerative disease myotonic dystrophy. The Drosophila muscleblind gene expresses four protein coding splice forms (mblA to mblD) that are differentially expressed during the Drosophila life cycle, and which vary markedly in their ability to rescue the embryonic lethal phenotype of muscleblind mutant flies. Analysis of muscleblind mutant embryos reveals misregulated alternative sp…

Gene isoformCancer ResearchMolecular Sequence DataBiologyKidneyChlorocebus aethiopsAnimalsDrosophila ProteinsHumansProtein IsoformsActininMuscle Skeletal3' Untranslated RegionsMolecular BiologyGeneCells CulturedCell NucleusGeneticsBase SequenceAlternative splicingGene Expression Regulation DevelopmentalNuclear ProteinsRNA-Binding ProteinsRNAKidney metabolismCell BiologyAlternative SplicingDrosophila melanogasterCOS CellsMutationRNA splicingTrinucleotide Repeat ExpansionTrinucleotide repeat expansionDevelopmental BiologyMinigeneDifferentiation
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Evidence for a common origin of most Friedreich ataxia chromosomes in the Spanish population

1996

Haplotype analysis is a powerful approach to understand the spectrum of mutations accounting for a disease in a homogeneous population. We show that haplotype variation for 10 markers linked to the Friedreich ataxia locus (FRDA) argues in favor of an important mutation homogeneity in the Spanish population, and positions the FRDA locus in the region where it has been recently isolated. We also report the finding of a new single nucleotide polymorphism called FAD1. The new marker shows a very strong linkage disequilibrium with Friedreich ataxia (FA) in both the Spanish and French populations. suggesting the existence of an ancient and widespread FRDA mutations. Inclusion of FAD1 in the exten…

Genetic MarkersLinkage disequilibriumAtaxiaMolecular Sequence DataPopulationNerve Tissue ProteinsSingle-nucleotide polymorphismLocus (genetics)BiologyLinkage DisequilibriumTrinucleotide RepeatsGeneticsmedicineHumanseducationPhylogenyGenetics (clinical)Adaptor Proteins Signal TransducingGeneticseducation.field_of_studyPolymorphism GeneticBase SequenceHaplotypeIntronChromosome MappingIntronsHaplotypesFriedreich AtaxiaSpainGenetic markerMutationFrancemedicine.symptom
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Isolation and characterization of 10 highly polymorphic di- and trinucleotide microsatellite markers in the mayfly Ameletus inopinatus (Ephemeroptera…

2008

We describe the isolation of ten polymorphic microsatellite loci from the mayfly Ameletus inopinatus. Loci had di- or trinucleotide repeat motifs and were highly variable with three to 17 alleles (mean = 7.15). Observed heterozygosity ranged from 0.143 to 0.905. One locus (Ami_202) showed significant deviation from Hardy–Weinberg equilibrium in one population, but no evidence for null alleles. One locus (Ami_73) was significantly linked with three other loci. The remaining nine loci should prove highly informative for population genetic studies.

Geneticseducation.field_of_studyPopulationLocus (genetics)Biologybiology.organism_classificationNull alleleLoss of heterozygosityMayflyGeneticsMicrosatelliteeducationTrinucleotide repeat expansionMicrosatellite enrichmentEcology Evolution Behavior and SystematicsBiotechnologyMolecular ecology resources
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ATNX2 is not a regulatory gene in Italian amyotrophic lateral sclerosis patients with C9ORF72 GGGGCC expansion

2015

Abstract There are indications that both familial amyotrophic lateral sclerosis (ALS) and sporadic ALS phenotype and prognosis are partly regulated by genetic and environmental factors, supporting the theory that ALS is a multifactorial disease. The aim of this article was to assess the role of ATXN2 intermediate length repeats in a large series of Italian and Sardinian ALS patients and controls carrying a pathogenetic C9ORF72 GGGGCC hexanucleotide repeat. A total of 1972 ALS cases were identified through the database of the Italian ALS Genetic consortium, a collaborative effort including 18 ALS centers throughout Italy. The study population included: (1) 276 Italian and 57 Sardinian ALS ca…

Male0301 basic medicineAgingC9ORF72Genetic Association Studie030105 genetics & heredityBiologySettore MED/03 - GENETICA MEDICA03 medical and health sciences0302 clinical medicineC9orf72medicineAlleleAmyotrophic lateral sclerosisAmyotrophic lateral sclerosiAgedAtaxin-2Regulator geneAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neuroscience (all); Medicine (all); Aging; Developmental Biology; Geriatrics and Gerontology; Neurology (clinical)GeneticsDNA Repeat ExpansionNeuroscience (all)ProteinMedicine (all)General NeuroscienceATXN2Middle AgedDNA Repeat Expansionmedicine.diseaseAmyotrophic lateral sclerosis3. Good healthC9orf72 ProteinAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyPhenotypeItalyPopulation studyFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyTrinucleotide repeat expansion030217 neurology & neurosurgeryHumanDevelopmental Biology
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Inheritance patterns of ATCCT repeat interruptions in spinocerebellar ataxia type 10 (SCA10) expansions

2017

Spinocerebellar ataxia type 10 (SCA10), an autosomal dominant cerebellar ataxia disorder, is caused by a non-coding ATTCT microsatellite repeat expansion in the ataxin 10 gene. In a subset of SCA10 families, the 5'-end of the repeat expansion contains a complex sequence of penta- and heptanucleotide interruption motifs which is followed by a pure tract of tandem ATCCT repeats of unknown length at its 3'-end. Intriguingly, expansions that carry these interruption motifs correlate with an epileptic seizure phenotype and are unstable despite the theory that interruptions are expected to stabilize expanded repeats. To examine the apparent contradiction of unstable, interruption-positive SCA10 e…

Male0301 basic medicineMolecular biologyInheritance Patternslcsh:MedicineGene ExpressionArtificial Gene Amplification and ExtensionPolymerase Chain ReactionDatabase and Informatics MethodsSequencing techniquesAutosomal dominant cerebellar ataxiaMedicine and Health SciencesDNA sequencinglcsh:ScienceGeneticsMovement DisordersMultidisciplinaryNeurodegenerative DiseasesGenomicsPedigreePhenotypeNeurologyMutation (genetic algorithm)Spinocerebellar ataxiaFemaleSequence AnalysisResearch ArticleBioinformaticsBiologyAtaxin-1003 medical and health sciencesSequence Motif AnalysisMicrosatellite RepeatGeneticsmedicineHumansSpinocerebellar AtaxiasRepeated SequencesAlleleAllelesSequence (medicine)EpilepsyBase SequenceBiology and life scienceslcsh:RDideoxy DNA sequencingGenetic Variationmedicine.diseaseResearch and analysis methodsMolecular biology techniques030104 developmental biologyTandem Repeat Sequence AnalysisAtaxinMutationlcsh:QAtaxiaTrinucleotide repeat expansionMicrosatellite RepeatsPLOS ONE
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Differential expression of PGC-1α and metabolic sensors suggest age-dependent induction of mitochondrial biogenesis in Friedreich ataxia fibroblasts.

2011

11 pages, 6 figures. PMID:21687738[PubMed] PMCID: PMC3110204

MaleAgingMitochondrial DiseasesMitochondrial MyopathyUbiquinoneCardiomyopathylcsh:MedicineMitochondrionAMP-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAntioxidantsAdenosine TriphosphateAMP-activated protein kinaseTrinucleotide RepeatsFibrosisMolecular Cell BiologyChildlcsh:ScienceHeat-Shock ProteinsRegulation of gene expressionMultidisciplinaryMovement DisordersbiologyNeuromuscular DiseasesMiddle AgedCatalasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyMitochondriaDNA-Binding ProteinsNeurologyDisease ProgressionMedicineFemalemedicine.symptomSignal TransductionResearch ArticleAdultcongenital hereditary and neonatal diseases and abnormalitiesAtaxiaAdolescentMitochondrial ProteinsmedicineGeneticsHumansBiologyAllelesGlutathione PeroxidaseSuperoxide Dismutaselcsh:RHuman GeneticsFibroblastsmedicine.diseaseMolecular biologyOxidative StressMitochondrial biogenesisGene Expression RegulationFriedreich Ataxiabiology.proteinFrataxinlcsh:QEnergy MetabolismReactive Oxygen SpeciesTranscription FactorsPLoS ONE
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