Search results for "Metachromatic leukodystrophy"

showing 8 items of 8 documents

A morphometric study on sural nerves in metachromatic leucodystrophy.

1987

This study reexamines peripheral neuropathy in infantile, juvenile and adult metachromatic leuco-dystrophy. A computer-assisted method was used which gives more detailed information on abnormal fibre structure from scatter diagrams of the g ratio (axon diameter/fibre diameter). The data show marked and statistically significant reductions in sheath thickness, particularly for the thick myelinated fibres, and most severe in the juvenile and adult forms. This is interpreted as evidence of remodelling of virtually the entire fibre population, without a clear-cut selectivity for either thin or thick fibres.

AdultAdolescentPopulationSural nerveNerve Fibers Myelinated03 medical and health sciences0302 clinical medicineSural NerveMedicineJuvenileHumansAxoneducationMyelin Sheath030304 developmental biologyMetachromatic leucodystrophy0303 health scienceseducation.field_of_studybusiness.industryInfantAnatomyLeukodystrophy Metachromaticmedicine.diseaseAxonsMetachromatic leukodystrophyMicroscopy Electronmedicine.anatomical_structurePeripheral neuropathySpinal NervesMyelin sheathNeurology (clinical)business030217 neurology & neurosurgerySoftwareBrain : a journal of neurology
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Sulfatide excreting heterozygous carrier of juvenile metachromatic leukodystrophy or asymptomatic patient of adult metachromatic leukodystrophy.

1975

In a family with juvenile metachromatic leukodystrophy (sulfatide lipidosis) 2 patients showed residual arysulfatase A activities of 5--6%. The patients' healthy father was characterized biochemically by a 39% normal activity of leukocyte plus plasma arylsulfatase A. The father was further characterized by a high sulfatide excretion (0.2--0.5 mg/I urine) and, paradoxically, by a normal sulfatide degrading enzyme activity in vitro. This special carrier is suspected to be heterozygous for a) arylsulfatase A deficiency and b) arylsulfatase A (sulfatidase) lability. This presumed additional genetic defect could be the cause of the sulfatide excretion which, in turn, would be a sign of the precl…

AdultMalemedicine.medical_specialtyArylsulfatase AHeterozygoteUrineBiologyAsymptomaticExcretionDrug StabilityInternal medicineGeneticsmedicineHumansChildGenetics (clinical)ArylsulfatasesSulfoglycosphingolipidsLeukodystrophy Metachromaticmedicine.diseaseEnzyme assayIn vitroMetachromatic leukodystrophyEnzyme ActivationEndocrinologybiology.proteinFemalemedicine.symptomSulfatasesArylsulfataseHumangenetik
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Retinopathia Pigmentosa Plus - the Value of Ultra-Structural Examination of the Human Retina

1993

Retinopathia pigmentosa is more widely, but somewhat incorrectly known as Retinitis pigmentosa (RP). Its course as a primary exclusively retinal disease follows autosomal-dominant, autosomal-recessive, or X-linked recessive modes of inheritance, or it may be sporadic. However, a progressive retinopathy, also called tapeto-retinal degeneration, may also be associated with numerous disorders: retinopathia pigmentosa plus (RPP). Among these RPP are those which form part of certain syndromes, e.g. Laurence-Moon-Bardet-Biedl syndrome, the Hallgren syndrome, the Marinesco-Sjogren syndrome, to name a few. Other RPP are associated with disorders of different organs, the skin, e.g. Werner disease, t…

Marfan syndromePathologymedicine.medical_specialtybusiness.industryOsteopetrosisDiseasemedicine.diseaseMyotonic dystrophyMetachromatic leukodystrophyNephronophthisisRetinitis pigmentosamedicinebusinessRetinopathy
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Preliminary clinical efficacy and safety of BMN 701, GILT-tagged recombinant human acid alpha glucosidase (rhGAA), in late-onset Pompe disease: resul…

2014

Metachromatic leukodystrophy (MLD) is a lysosomal disorder that results from the deficiency of the lysosomal enzyme arylsulfatase A. It is characterized by motor and developmental regression, seizures, deafness, blindness, dementia and premature death. There are three types of onsets: late infantile, juvenile, and adult. We performed a retrospective chart review of 71 patients (47 infantile, 23 juvenile) evaluated at the Program for Study of Neurodevelopment in Rare Disorders (NDRD) between January 2000 and August 2013. The patients were evaluated prospectively using a standardized protocol. The purpose of the study is to describe the natural course of the disease. In 31 patients only a bas…

Newborn screeningPediatricsmedicine.medical_specialtybusiness.industryEndocrinology Diabetes and MetabolismLate onsetDiseasemedicine.diseaseBiochemistryVirologyMetachromatic leukodystrophyEndocrinologyGeneticsmedicineDementiaJuvenileAge of onsetbusinessMolecular BiologyDevelopmental regressionMolecular Genetics and Metabolism
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Intraepidermal morphologic manifestations in lysosomal diseases.

1989

This paper reports the ultrastructural findings for the epidermis of biopsied skin specimens in numerous lysosomal diseases, which can be grouped as follows: a) presence of vacuolar lysosomal residual bodies in mucopolysaccharidoses I, II and III, Salla disease, GM 2 -gangliosidoses and infantile type II glycogenosis; b) avacuolar lysosomal residual bodies in Niemann-Pick disease type C, mucolipidosis IV, Farber disease, Fabry disease, and late infantile and juvenile neuronal ceroid-lipofuscinoses; c) absence of lysosomal residual bodies in GM 2 -gangliosidoses, metachromatic leukodystrophy, Gaucher disease and sialidosis type III Whenever possible, a biopsy of the skin for morphological di…

Pathologymedicine.medical_specialtyBiologyGangliosidosesDevelopmental NeuroscienceLysosomeBiopsymedicineHumansSialidosisSkinInclusion BodiesFarber diseasemedicine.diagnostic_testGeneral Medicinemedicine.diseaseFabry diseaseMetachromatic leukodystrophyMicroscopy Electronmedicine.anatomical_structureSalla diseasePediatrics Perinatology and Child HealthImmunologyNeurology (clinical)LysosomesMetabolism Inborn ErrorsBraindevelopment
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ALTERED RATIO BETWEEN AXON CALIBER AND MYELIN THICKNESS IN SURAL NERVES OF CHILDREN

1978

ABSTRACT Maturation of myelin sheaths in normal sural nerves of children proceeds more slowly than axon growth. This asynchronous development of axons and myelin sheaths results in a statistically significant change of the ratio between axon caliber and myelin thickness during normal development. Therefore, myelin thickness of individual nerve fibers must be related to the size of the axons as well as to the age of the individuals studied. Abnormalities of the relationship between myelin thickness and axon diameter (primary hypomyelination of large, or small, or all fibers) were clearly identified in cases with metachromatic leukodystrophy, KRABBE's, DEJERINE-SOTTAS’, COCKAYNE'S and SANFILI…

Peripheral myelinAnatomyGangliosidosisBiologymedicine.diseaseAxon growthMetachromatic leukodystrophyMyelinmedicine.anatomical_structurenervous systemCaliberCeroid lipofuscinosismedicineAxon
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Ultrastructural study of the retina in late infantile metachromatic leukodystrophy.

1992

The autopsy of a 2-year-old girl revealed a clinically unrecognized metachromatic leukodystrophy (MLD) due to an aryl-sulfatase A deficiency, characteristically affecting the central and peripheral nervous system by demyelination and by accumulation of metachromatic material. The retina though reported clinically as normal, showed the same demyelinating process in the optic nerve including the papilla but an additional intraneuronal storage of MLD-typical lysosomal residual bodies in ganglion cell perikarya of the retina. Cells of the bipolar and photoreceptor layers as well as pigment epithelial cells were not affected by MLD-specific lysosomal storage. Thus, sulfatides seem to play a part…

Retinal Ganglion CellsPathologymedicine.medical_specialtyAutopsyBiologycomplex mixturesRetinaCellular and Molecular NeuroscienceRetinal DiseasesmedicineHumansRetinaBrainGeneral MedicineLeukodystrophy Metachromaticmedicine.diseaseeye diseasesSensory SystemsGanglionMajor duodenal papillaMetachromatic leukodystrophyOphthalmologymedicine.anatomical_structurePeripheral nervous systemChild PreschoolOptic nerveUltrastructureFemalesense organsLysosomesOphthalmic research
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Abnormal Lipopigments and Lysosomal Residual Bodies in Metachromatic Leukodystrophy

1990

Ultrastructurally, metachromatic leukodystrophy (MLD) is marked by characteristic features such as herringbone, prismatic and tufaceous patterns which are typically encountered within oligodendrocytes of the central nervous system (CNS) and in Schwann cells (PNS). These patterns can be documented in late infantile, juvenile, and adult forms. In the latter, aging of the ailing individual adds another component, the accumulation of lipopigments which are marked by an opaque supposedly lipid droplet and a granular component. While MLD-specific lysosomal residual bodies occur in myelinforming cells, lipopigments accrue in neurons and to a lesser degree in astrocytes. MLD represents a unique exa…

education.field_of_studyCell typePathologymedicine.medical_specialtyPopulationCentral nervous systemResidual bodyBiologymedicine.diseasecomplex mixturesMetachromatic leukodystrophymedicine.anatomical_structureLipid dropletSweat glandmedicineGranular componenteducation
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