Search results for "Motor Neuron"

showing 10 items of 140 documents

Homozygous SMN1 exons 1-6 deletion: pitfalls in genetic counseling and general recommendations for spinal muscular atrophy molecular diagnosis.

2012

We report on a rare homozygous intragenic deletion encompassing exons 1-6 of the SMN1 gene in a patient with spinal muscular atrophy (SMA) born into a consanguineous family. This exceptional configuration induced misinterpretation of the molecular defect involved in this patient, who was first reported as having a classic SMN1 exon 7 deletion. This case points out the possible pitfalls in molecular diagnosis of SMA in affected patients and their relatives: exploration of the SMN1 exon 7 (c.840C/T alleles) may be disturbed by several non-pathological or pathological variants around the SMN1 exon 7. In order to accurately describe the molecular defect in an SMA-affected patient, we propose to…

Genetic counselingGenetic CounselingSMN1BiologyMuscular Atrophy SpinalExonGeneticsmedicineHumansAlleleGeneGenetics (clinical)AllelesGeneticsHomozygoteChromosome MappingInfantSpinal muscular atrophyExonsmedicine.diseaseSMA*Survival of Motor Neuron 1 Proteinnervous system diseasesPedigreeHuman genomeFemaleGene DeletionAmerican journal of medical genetics. Part A
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Carrier screening for spinal muscular atrophy in Italian population

2014

Spinal muscular atrophy (SMA) is an autosomal-recessive neuromuscular disorder characterized by motor neuron degeneration in the anterior horn of the spinal cord and brain stem, resulting in progressive muscle weakness and atrophy. The responsible survival motor neuron gene (SMN1; HGNC: 11117) is localized in 5q11.2-13.3. Screening for carriers of SMA is necessary for effective clinical/prenatal diagnosis and genetic counselling. In this study, the copy number of SMN1 gene was determined from a southern Italian population to estimate carrier frequency. This is the first report addressing the estimation of SMA carrier frequency in an Italian population. Our results show that the SMA carrier …

HeterozygoteGenetic counselingGene DosagePhysiologycarrier screeningPrenatal diagnosisSMN1BiologyCarrier testingMuscular Atrophy SpinalAtrophyGene FrequencySettore BIO/13 - Biologia ApplicataPrevalenceGeneticsmedicineHumansGenetic Testingspinal muscular atrophysurvival motor neuron gene (SMN1); spinal muscular atrophy; carrier screening; MLPAExonsSpinal muscular atrophyMotor neuronSMA*medicine.diseaseSurvival of Motor Neuron 1 ProteinMLPAmedicine.anatomical_structureItalysurvival motor neuron gene (SMN1)Journal of Genetics
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Quantitative image analysis of the chromatolysis in rat facial and hypoglossal motoneurons following axotomy with and without reinnervation.

1996

Image analysis was used to quantify the time course of chromatolysis in regenerating and degenerating motoneurons. Following facial-facial, hypoglossal-hypoglossal nerve suture, or resection of facial and hypoglossal nerves with postoperative survival times of 4 h to 112 days, the texture of the Nissl substance of facial and hypoglossal motoneurons was analyzed on both sides of the brainstem in paraffin serial sections with a VIDASplus image analyzer. In this quantitative study of 149 Wistar rats, alterations of the Nissl substance were measured that were statistically significant but not yet visible to the human eye. Chromatolysis started significantly as early as 8 h and was not fully rev…

Hypoglossal NerveHistologyTime Factorsmedicine.medical_treatmentPathology and Forensic Medicinesymbols.namesakemedicineImage Processing Computer-AssistedAnimalsRats WistarMotor Neuronsbusiness.industryCell BiologyAnatomyFacial nerveAxonsNerve RegenerationRatsFacial Nervemedicine.anatomical_structurenervous systemNissl BodiesChromatolysisTime courseNerve DegenerationNissl bodysymbolsFemaleBrainstemAxotomybusinessHypoglossal nerveReinnervationCell and tissue research
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The use of texture analysis to study the time course of chromatolysis

1998

Image analysis of the textural feature entropy of the Nissl substance was used to monitor the time course of chromatolysis in regenerating hypoglossal motoneurons and degenerating facial motoneurons 4-112 days after hypoglossal-facial anastomosis in rats. Changes in the Nissl substance were detected that were not obvious on the basis of subjective judgement of the light-microscopical appearance of the neurons. Chromatolysis started 4 days post operation (dpo) and was not reversed at 112 dpo in both nuclei. The increase of chromatolysis was 14-28 dpo faster in the regenerating hypoglossal neurons than in degenerating facial neurons. Maximal chromatolysis was measured at 56-70 dpo in both nuc…

Hypoglossal NerveTime FactorsEntropyBiologysymbols.namesakeImage Processing Computer-AssistedmedicineAnimalsRats WistarMotor NeuronsGeneral NeuroscienceAnastomosis SurgicalAnatomyMotor neuronFacial nerveNerve RegenerationRatsFacial Nervemedicine.anatomical_structurenervous systemNissl BodiesChromatolysisTime courseNissl bodysymbolsFemaleNeuronNeuronal cell bodyNeuroscienceHypoglossal nerveJournal of Neuroscience Methods
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Post-translational modifications in the survival motor neuron protein

2004

Spinal muscular atrophy (SMA) is an autosomal recessive disease characterized by a progressive loss of the spinal motoneurons. The SMA-determining gene has been termed survival motor neuron (SMN) and is deleted or mutated in over 98% of patients. The encoded gene product is a protein expressed as different isoforms. In particular, we showed that the rat SMN cDNA produces two isoforms with Mr of 32 and 35 kDa, both localized in nuclear coiled bodies, but the 32 kDa form is also cytoplasmic, whereas the 35 kDa form is also microsomal. To determine the molecular relationship between these two isoforms and potential post-translational modifications, we performed transfection experiments with a …

INVOLVEMENTFORMSPRODUCTBiochemistryMiceChlorocebus aethiopsProtein IsoformsPhosphorylationCyclic AMP Response Element-Binding ProteinSMN PROTEINCells CulturedMotor NeuronsSPINAL MUSCULAR-ATROPHYRNA-Binding ProteinsSMN Complex Proteins3T3 CellsTransfectionmedicine.anatomical_structureSpinal CordCOS CellsSUBCELLULAR-LOCALIZATIONEXPRESSIONGene isoformRecombinant Fusion ProteinsBiophysicsNerve Tissue ProteinsBiologyMuscular Atrophy SpinalGene productSMN Complex ProteinsComplementary DNAmedicineAnimalsHumansMolecular BiologyCell BiologySpinal muscular atrophyMotor neuronmedicine.diseaseSurvival of Motor Neuron 1 ProteinMolecular biologyRatsnervous system diseasesMolecular WeightSEVERITYnervous systemBODIESProtein Processing Post-TranslationalDETERMINING GENEImmunostainingBiochemical and Biophysical Research Communications
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Hirayama disease: Nosological classification and neuroimaging clues for diagnosis

2022

Hirayama disease (HD) is a rare, benign, and nonprogressive motor neuron disease (MND) affecting the upper limbs. It usually presents with weakness and amyotrophy in a single upper extremity with an insidious onset between adolescence and the third decade of life. Since its description in 1959, HD has been known under several names and eponyms in Europe and in Asian countries probably due to its heterogeneous clinical features. Thus, the unclear nosological classification makes challenging the differential diagnosis between HD and other neuromuscular conditions, such as MNDs. However, apart from the nosological difficulties and the lack of evidence-based guideline for diagnosis, the neuroim…

MaleAdolescentNeuroimagingSpinal Muscular Atrophies of ChildhoodJASSMAMagnetic Resonance Imagingcervical MRImotor neuron diseaseHumansRadiology Nuclear Medicine and imagingNeurology (clinical)MMANeckflexion MRIHirayama
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Mutations in ATP13A2 (PARK9) are associated with an amyotrophic lateral sclerosis-like phenotype, implicating this locus in further phenotypic expans…

2019

Background Amyotrophic lateral sclerosis [1] is a genetically heterogeneous neurodegenerative disorder, characterized by late-onset degeneration of motor neurons leading to progressive limb and bulbar weakness, as well as of the respiratory muscles, which is the primary cause of disease fatality. To date, over 25 genes have been implicated as causative in ALS with C9orf72, SOD1, FUS, and TARDBP accounting for the majority of genetically positive cases. Results We identified two patients of Italian and French ancestry with a clinical diagnosis of juvenile-onset ALS who were mutation-negative in any of the known ALS causative genes. Starting with the index case, a consanguineous family of Ita…

MaleAmyotrophic lateral sclerosis ATP13A2 parkinsonismlcsh:Medicine0302 clinical medicineC9orf72Drug DiscoveryAmyotrophic lateral sclerosisIndex caseZebrafishExome sequencingMotor NeuronsGenetics0303 health sciencesDEMENTIA1184 Genetics developmental biology physiologyMiddle AgedPedigree3. Good healthProton-Translocating ATPasesPhenotypeMolecular MedicineFemaleSettore MED/26 - NeurologiaPrimary ResearchAdultlcsh:QH426-470SOD1BiologyTARDBP03 medical and health sciencesParkinsonian DisordersNeuronal Ceroid-LipofuscinosesExome SequencingGeneticsmedicineAnimalsHumansGenetic Predisposition to DiseaseMolecular Biology030304 developmental biologyGenetic heterogeneityAmyotrophic Lateral Sclerosislcsh:Rmedicine.diseaseDisease Models Animallcsh:GeneticsMutationNeuronal ceroid lipofuscinosis030217 neurology & neurosurgeryPARKINSONISM
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Absence of an aging-related increase in fiber type grouping in athletes and non-athletes

2020

The ageing-related loss of muscle mass is thought to be partly attributable to motor neuron loss and motor unit remodelling that result in fibre type grouping. We examined fibre type grouping in 19- to 85-year-old athletes and non-athletes and evaluated to which extent any observed grouping is explained by the fibre type composition of the muscle. Since regular physical activity may stimulate reinnervation, we hypothesised that fibre groups are larger in master athletes than in age-matched non-athletes. Fibre type grouping was assessed in m. vastus lateralis biopsies from 22 young (19-27 years) and 35 healthy older (66-82 years) non-athletes, and 14 young (20-29 years), 51 middle-aged (38%6…

MaleBiopsy030204 cardiovascular system & hematologyMuskel- und KnochenstoffwechselQuadriceps Muscleudc:612.74:612.660302 clinical medicinegroupingOrthopedics and Sports MedicineFibre typeAged 80 and overMotor NeuronsDenervationbiologyFiber typestaranjemišična vlaknaMiddle Agedfibre typeMuscle Fibers Slow-Twitchmedicine.anatomical_structureMuscle Fibers Fast-TwitchreinervacijaFemaleSportsReinnervationAdultmedicine.medical_specialtyPhysical Therapy Sports Therapy and RehabilitationYoung Adult03 medical and health sciencesInternal medicinevastus lateralismedicineHumansAgeddenervationbusiness.industryAthletesaging030229 sport sciencesMotor neuronbiology.organism_classificationfiber typereinnervationMotor unitdenervacijaCross-Sectional StudiesEndocrinologyAgeingbusiness
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Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing

2021

AbstractMotoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and …

MaleCancer ResearchPhysiology129 StrainBiochemistryMiceDatabases GeneticMedicineMyocyteMotor NeuronsNeuronal PlasticitySkeletalSmoothened ReceptorHedgehog signaling pathwayMuscle atrophyMitochondriaAstrogliosisNeuroprotective AgentsMusclemedicine.symptomInflammation MediatorsSignal TransductionCholera ToxinMice 129 StrainhedgehogImmunologyMotor ActivityNeuroprotectionArticleDatabasesCellular and Molecular NeurosciencesmoothenedGeneticAnimalsHumansHedgehog ProteinsMuscle SkeletalHedgehogGlucocorticoidsMuscle DenervationQH573-671Animalbusiness.industryAmyotrophic Lateral SclerosisGlial biologyCell Biologymedicine.diseaseSaporinsSpineMitochondria MuscleDisease Models AnimalclobetasolinflammationCase-Control StudiesDisease ModelsDiseases of the nervous systemCytologySmoothenedbusinessEnergy MetabolismNeuroscienceOpen Field Test
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Aberrant arrested in maturation neuromuscular junctions in centronuclear myopathy

1994

Unusual ultrastructural changes of the nerve terminals have been found in an infant born with severe, fatal XLR form of centronuclear myopathy. Aberrant neuromuscular junctions in myotubes decorated by N-CAM were observed. The junction changes were manifested by simplification of postsynaptic membrane and paucity of secondary synaptic clefts. These resembles fetal neuromuscular junctions. The findings suggest that the expression of N-CAM by arrested myotubes may be promoted by abnormal nerve-muscle cell interactions, induced by motor endplate immaturity.

MaleCell Adhesion Molecules NeuronalCellNeuromuscular JunctionElectromyographyBiologyMicrotubulesMotor EndplateNeuromuscular junctionMotor EndplateMicrotubulemedicineHumansCentronuclear myopathyMotor NeuronsFetusTissue Embeddingmedicine.diagnostic_testElectromyographyMyogenesisMusclesInfantNeuromuscular Diseasesmedicine.diseaseCell biologyMicroscopy Electronmedicine.anatomical_structureNeurologySynapsesNeurology (clinical)NeuroscienceJournal of the Neurological Sciences
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