Search results for "Leigh Disease"

showing 3 items of 3 documents

Sural nerve biopsy studies in leigh's subacute necrotizing encephalomyelopathy

1986

Peripheral neuropathy marked by reduced nerve conduction velocities was found in four unrelated children, between the ages of 15 months and 9 years, whose autopsies revealed Leigh's subacute necrotizing encephalomyelopathy. Sural nerve biopsies disclosed primary demyelination and remyelination, as well as loss of myelinated and unmyelinated axons. The use of morphometric and electron microscopic studies shows that these techniques may reveal peripheral neuropathy in Leigh's disease more often than light microscopic methods alone.

0303 health sciencesPathologymedicine.medical_specialtymedicine.diagnostic_testPhysiologyPrimary demyelinationbusiness.industrySural nerveSural nerve biopsymedicine.disease03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicine.anatomical_structurePeripheral neuropathyPhysiology (medical)BiopsymedicineNeurology (clinical)RemyelinationLeigh diseasebusinessElectron microscopic030217 neurology & neurosurgery030304 developmental biologyMuscle & Nerve
researchProduct

Leigh syndrome due to compound heterozygosity of dihydrolipoamide dehydrogenase gene mutations. Description of the first E3 splice site mutation.

2003

Item does not contain fulltext A boy with recurrent episodes of hypoglycaemia and ataxia, microcephaly, mental retardation, permanent lactic acidaemia, intermittent 2-oxoglutaric aciduria as well as elevation of serum branched chain amino acids was diagnosed with dihydrolipoamide dehydrogenase (E3) deficiency. Analysis of genomic DNA revealed compound heterozygosity for two novel mutations: I393T in exon 11, located at the interface domain of the protein and possibly interfering with its dimerisation, and IVS9+1G>A located at a consensus splice site. A heterozygous polymorphism was also detected. In the patient's cDNA the I393T mutation and the polymorphism appeared to be homozygous, indica…

MaleHeterozygoteMutation MissensePyruvate Dehydrogenase ComplexGene mutationBiologyCompound heterozygosityLoss of heterozygositymedicineHumansLeigh diseaseMuscle SkeletalDihydrolipoamide DehydrogenaseGeneticsSplice site mutationDihydrolipoamide dehydrogenasePyruvate Dehydrogenase (Lipoamide)Fibroblastsmedicine.diseasePyruvate dehydrogenase complexRenal disorders [UMCN 5.4]Genetic defects of metabolism [UMCN 5.1]Child PreschoolPediatrics Perinatology and Child HealthRNA Splice SitesLeigh DiseaseCellular energy metabolism [UMCN 5.3]
researchProduct

Novel LRPPRC compound heterozygous mutation in a child with early-onset Leigh syndrome French-Canadian type: Case report of an Italian patient

2020

Abstract Background Mitochondrial diseases, also known as oxidative phosphorylation (OXPHOS) disorders, with a prevalence rate of 1:5000, are the most frequent inherited metabolic diseases. Leigh Syndrome French Canadian type (LSFC), is caused by mutations in the nuclear gene (2p16) leucine-rich pentatricopeptide repeat-containing (LRPPRC). It is an autosomal recessive neurogenetic OXPHOS disorder, phenotypically distinct from other types of Leigh syndrome, with a carrier frequency up to 1:23 and an incidence of 1:2063 in the Saguenay-Lac-St Jean region of Quebec. Recently, LSFC has also been reported outside the French-Canadian population. Patient presentation We report a male Italian (Sic…

MaleHypotonia - developmental delayPediatricsmedicine.medical_specialtyPopulationEncephalopathyCytochrome-c Oxidase DeficiencyCase ReportHypotoniaCompound heterozygosityDiagnosis Differential03 medical and health sciences0302 clinical medicineWhole-genome-sequencingHypotonia; developmental delay; Mitochondrial disease; Whole-exome sequencing; CCT5030225 pediatricsmedicineMissense mutationHumansGlobal developmental delayeducationeducation.field_of_studyComparative Genomic Hybridizationbusiness.industrylcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseHypotoniaHypoplasiaMitochondrial diseaseNeoplasm Proteinsdevelopmental delayNeonatal hypotoniaPhenotypeItalyWhole-exome sequencingMutationLSFCmedicine.symptomLeigh DiseaseCCT5business030217 neurology & neurosurgeryInfant Premature
researchProduct