Search results for "ATAXIAS"

showing 10 items of 12 documents

Comparative multiplex dosage analysis in spinocerebellar ataxia type 2 patients.

2013

We developed a new application of comparative multiplex dosage analysis (CMDA) for evaluation of the ataxin 2 gene. Expansions of the triplet CAG can cause spinocerebellar ataxia type 2 (SCA2), a neurodegenerative disease with an autosomal-dominant mode of inheritance. Molecular diagnosis of SCA2 is routinely based on the use of conventional PCR to detect the CAG expansion. However, PCR does not amplify an allele with an expansion of many triplets (>80), which is typically found in infantile and juvenile forms of SCA2, thus leading to false negatives. We propose the analysis of the ATXN2 gene by CMDA to complement existing methods currently used for the detection of large expansions of the …

Malecongenital hereditary and neonatal diseases and abnormalitiesGenotypeGene DosagePrenatal diagnosisNerve Tissue ProteinsDiseaseAtaxin 2 Spinocerebellar ataxia type 2 Quantitative PCR Autosomal dominant Prenatal diagnosisSettore BIO/13 - Biologia ApplicataGeneticsMedicineHumansSpinocerebellar AtaxiasMultiplexAlleleMolecular BiologyGeneAllelesGeneticsbusiness.industryGeneral Medicinemedicine.diseaseReal-time polymerase chain reactionAtaxinsAtaxinCase-Control StudiesSpinocerebellar ataxiaFemalebusinessTrinucleotide Repeat ExpansionMultiplex Polymerase Chain ReactionGenetics and molecular research : GMR
researchProduct

Polyglutamine toxicity induces rod photoreceptor division, morphological transformation or death in Spinocerebellar ataxia 7 mouse retina

2010

In neurodegenerative disorders caused by polyglutamine (polyQ) expansion, polyQ toxicity is thought to trigger a linear cascade of successive degenerative events leading to neuronal death. To understand how neurons cope with polyQ toxicity, we studied a Spinocerebellar ataxia 7 (SCA7) mouse which expresses polyQ-expanded ATXN7 only in rod photoreceptors. We show that in response to polyQ toxicity, SCA7 rods go through a range of radically different cell fates, including apoptotic and non-apoptotic cell death, cell migration, morphological transformation into a round cell or, most remarkably, cell division. The temporal profile of retinal remodeling indicates that some degenerative pathways …

Programmed cell deathCell divisionProliferationPopulationMice TransgenicNerve Tissue ProteinsBiologylcsh:RC321-571Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell MovementRetinal Rod Photoreceptor CellsmedicineAnimalsSpinocerebellar AtaxiasNeurodegenerationeducationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCell ShapeComputingMilieux_MISCELLANEOUSSpinocerebellar ataxia 7030304 developmental biologyAtaxin-7Mice Knockout0303 health sciencesRetinaeducation.field_of_studyPhotoreceptorCell DeathRetinal DegenerationNeurodegenerationRetinalmedicine.diseaseRemodelingMice Inbred C57BLmedicine.anatomical_structureNeurologyProteotoxicitychemistryNerve DegenerationSpinocerebellar ataxia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Apoptosis Regulatory ProteinsPeptidesPolyglutamineNeuroscience030217 neurology & neurosurgery
researchProduct

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
researchProduct

Spinocerebellar ataxia: functional analysis of the stomatognathic system

2019

Background Neurodegenerative diseases that affect the cerebellum, especially in elderly individuals, cause impairment of motor coordination and quality of life. The presente study evaluated the electromyographic activity and thickness of the right and left masseter and temporal muscles, and the maximum molar bite force of individuals with spinocerebellar ataxia. Material and Methods Twenty-eight individuals were divided into two groups: those with (n=14) and without (n=14) spinocerebellar ataxia. Data on the masticatory muscles obtained from the electromyographic activity (resting, right and left laterality and protrusion), muscle thickness (maximal voluntary contraction and tensile strengt…

MolarAdultMaleCerebellumcongenital hereditary and neonatal diseases and abnormalitiesTemporal MuscleMandibleFunctional LateralityBite ForceDental OcclusionMedicineHumansSpinocerebellar AtaxiasProspective StudiesStomatognathic SystemGeneral DentistryOrthodonticsOral Medicine and PathologyDOENÇAS DEGENERATIVASbusiness.industryElectromyographyMasseter MuscleResearchMiddle AgedTemporomandibular Joint Disordersmedicine.disease:CIENCIAS MÉDICAS [UNESCO]MolarMasticatory forceMotor coordinationBite force quotientStomatognathic systemmedicine.anatomical_structureOtorhinolaryngologyCase-Control StudiesUNESCO::CIENCIAS MÉDICASLateralityMasticatory MusclesSpinocerebellar ataxiaQuality of LifeMasticationSurgeryFemalebusinessBrazil
researchProduct

Repeat expansion in spinocerebellar ataxia type 17 alleles of the TATA-box binding protein gene: an evolutionary approach.

2006

The variability and mutational changes of the CAG microsatellite in the TATA-box binding protein gene (TBP) were studied. We sequenced the microsatellite of the TBP gene of 25 unrelated individuals from northern Germany (10 SCA17 patients and 15 unaffected control individuals). In addition, the microsatellites were sequenced from individuals of 10 northern German families with at least one family member affected by SCA17. To study also the evolutionary history of this CAG/CAA microsatellite in nonhuman primates, the homologous regions were analysed from Pan troglodytes, Gorilla gorilla, Pongo pygmaeus, P. abellii, Hylobates lar, Nomascus leucogenys, Symphalangus syndactylus, Macaca mulatta,…

MalePrimatesUnequal crossing overEvolution MolecularMolecular evolutionHylobatesGeneticsmedicineAnimalsHumansSpinocerebellar AtaxiasComputer SimulationAlleleGenetics (clinical)GeneticsbiologyGenetic Variationbiology.organism_classificationmedicine.diseaseTATA-Box Binding ProteinNomascus leucogenysSpinocerebellar ataxiaMicrosatelliteFemaleTrinucleotide repeat expansionTrinucleotide Repeat ExpansionEuropean journal of human genetics : EJHG
researchProduct

SPG10 is a rare cause of spastic paraplegia in European families.

2008

Contains fulltext : 71099.pdf (Publisher’s version ) (Closed access) BACKGROUND: SPG10 is an autosomal dominant form of hereditary spastic paraplegia (HSP), which is caused by mutations in the neural kinesin heavy chain KIF5A gene, the neuronal motor of fast anterograde axonal transport. Only four mutations have been identified to date. OBJECTIVE: To determine the frequency of SPG10 in European families with HSP and to specify the SPG10 phenotype. PATIENTS AND METHODS: 80 index patients from families with autosomal dominant HSP were investigated for SPG10 mutations by direct sequencing of the KIF5A motor domain. Additionally, the whole gene was sequenced in 20 of these families. RESULTS: Th…

MaleDNA Mutational AnalysisKinesinsHEREDITARYmedicine.disease_cause0302 clinical medicineSpasticPerception and Action [DCN 1]Missense mutationKIF5AAge of OnsetChildFrameshift MutationMUTATIONGenes DominantGeneticsNeurologic Examination0303 health sciencesMutationSplice site mutationSITEExonsMiddle AgedAnterograde axonal transport3. Good healthPedigreeEuropePsychiatry and Mental healthPhenotypeATAXIASChild PreschoolFemaleChromosome DeletionMOTORFunctional Neurogenomics [DCN 2]AdultNeuromuscular diseaseGenotypeHereditary spastic paraplegiaMutation Missense03 medical and health sciencesCognitive neurosciences [UMCN 3.2]medicineHumansGait Disorders Neurologic030304 developmental biologyChromosome Aberrationsbusiness.industrySpastic Paraplegia HereditarySequence Analysis DNAmedicine.diseaseGENEPeripheral neuropathyGenetics PopulationSurgeryNeurology (clinical)RNA Splice Sitesbusiness030217 neurology & neurosurgeryJournal of neurology, neurosurgery, and psychiatry
researchProduct

Marinesco-Sjögren syndrome caused by a new SIL1 frameshift mutation

2015

no abstract available

Neurologybusiness.industryMarinesco–Sjögren syndromeAutosomal recessive cerebellar ataxias Cerebellar atrophy Early-onset cataracts Marinesco-Sjögren Syndrome Mental retardation SIL1 geneCancer researchMedicineCerebellar atrophySettore MED/26 - NeurologiaNeurology (clinical)businessmedicine.diseaseAutosomal recessive cerebellar ataxias; Cerebellar atrophy; Early-onset cataracts; Marinesco-Sjögren Syndrome; Mental retardation; SIL1 geneFrameshift mutation
researchProduct

Cognitive and social cognitive functioning in spinocerebellar ataxia : a preliminary characterization

2006

INTRODUCTION : The spinocerebellar ataxias (SCAs), are rare neurodegenerative disorders caused by distinct genetic mutations. Clinically, the SCAs are characterised by progressive ataxia and a variety of other features, including cognitive dysfunction. The latter is consistent with a growing body of evidence supporting a cognitive as well as motor role for the cerebellum. Recent suggestions of cerebellar involvement in social cognition have not been extensively explored in these conditions. The availability of definitive molecular diagnosis allows genetically defined subgroups of SCA patients, with distinct patterns of cerebellar and extracerebellar involvement, to be tested comparatively u…

AdultMaleEmotionsNeuropsychological TestsSocial Environmentcognitive functioningDisability EvaluationCognitionSocial cognitionCerebellumTheory of mindmedicineHumansSpinocerebellar AtaxiasCognitive skillSocial BehaviorAgedIntelligence TestsVerbal BehaviorCognitive disorderNeuropsychologyRecognition PsychologyCognitionMachado-Joseph DiseaseMiddle Agedmedicine.diseaseNeurologyMental RecallSpinocerebellar ataxiaAutismFemaleAtaxiaNeurology (clinical)PsychologyNeurosciencePsychomotor Performance
researchProduct

A longitudinal investigation into cognition and disease progression in spinocerebellar ataxia types 1, 2, 3, 6, and 7

2016

Background The natural history of clinical symptoms in the spinocerebellar ataxias (SCA)s has been well characterised. However there is little longitudinal data comparing cognitive changes in the most common SCA subtypes over time. The present study provides a preliminary longitudinal characterisation of the clinical and cognitive profiles in patients with SCA1, SCA2, SCA3, SCA6 and SCA7, with the aim of elucidating the role of the cerebellum in cognition. Methods 13 patients with different SCAs all caused by CAG repeat expansion (SCA1, n = 2; SCA2, n = 2; SCA3, n = 2; SCA6, n = 4; and SCA7, n = 3) completed a comprehensive battery of cognitive and mood assessments at two time points, a mea…

AdultMaleMedicine(all)Settore M-PSI/02 - Psicobiologia E Psicologia FisiologicaResearchNeuroimagingMiddle AgedCognitionNeuropsychologyDisease ProgressionHumansSpinocerebellar AtaxiasFemaleAtaxiaGenetics(clinical)Pharmacology (medical)Longitudinal StudiesSpinocerebellar ataxiaAgedAtaxia; Cognition; Spinocerebellar ataxiaOrphanet Journal of Rare Diseases
researchProduct

Incidentalome in Neurogenetics: Pathogenic Variant of NSD1 in a Patient With Spinocerebellar Ataxia (SCA)

2018

Background: Genetic studies of late-onset sporadic ataxias (>40 years of age) are not routinely indicated. For unresolved cases, next-generation sequencing (NGS) tools, such as whole-exome sequencing (WES), are available for a definitive diagnosis.Case presentation: Our patient is a woman with a usual facial phenotype and anthropometry, who developed ataxia at 45 years of age, with no relevant family history and an initial clinical approach that ruled out common aetiologies. WES was performed when the patient was 54 years old. The results identified the heterozygous pathogenic variant c.248delA (p.N83MfsX4) in the nuclear receptor-binding SET domain protein 1 (NSD1; MIM 606681) gene (rel…

0301 basic medicineAtaxialcsh:QH426-470Neurogeneticslate-onset sporadic ataxiasNSD103 medical and health sciencessymbols.namesakemedicineGeneticswhole-exome sequencingFamily historyGenetics (clinical)Exome sequencingGeneticsSanger sequencingSotos syndromebusiness.industrydiagnostics testmedicine.diseasePhenotypelcsh:Genetics030104 developmental biologyPerspectivegenetic incidentalomeSpinocerebellar ataxiasymbolsMolecular Medicinemedicine.symptombusinessFrontiers in Genetics
researchProduct