Search results for "Spastic Paraplegia"

showing 10 items of 23 documents

Mutation analysis of the SPG4 gene in Italian patients with pure and complicated forms of spastic paraplegia

2010

Mutations in the SPG4 gene are the most common causes of hereditary spastic paraplegia (HSP) accounting for up to 40% of autosomal dominant (AD) forms and 12-18% of sporadic cases. The phenotype associated with HSP due to mutations in the SPG4 gene tends to be pure. There is increasing evidence, however, of patients with complicated forms of spastic paraplegia in which SPG4 mutations were identified. A cohort of 38 unrelated Italian patients with spastic paraplegia, of which 24 had a clear dominant inheritance and 14 were apparently sporadic, were screened for mutations in the SPG4 gene.We identified 11 different mutations, six of which were novel (p.Glu143GlyfsX8, p.Tyr415X, p.Asp548Asn, c…

MaleSpastinDNA Mutational AnalysisHereditary spastic paraplegiaEXON DELETIONSGene mutationmedicine.disease_causeSpastinFAMILIESCohort StudiesExonGenotypeSpasticMutation frequencyChild3' Untranslated RegionsChromatography High Pressure LiquidAdenosine TriphosphatasesGeneticsMutationHereditary spastic paraplegia SPG4Reverse Transcriptase Polymerase Chain ReactionMutation analysiExonsMiddle AgedMLPAPhenotypeMutation analysisItalyNeurologySettore MED/26 - NeurologiaFemaleAdultAdolescentGenotypeHereditary spastic paraplegia3 ' UTR3′ UTRMutation MissenseFREQUENTSPG4CLASSIFICATIONYoung AdultmedicineHumansAgedParaplegiaSPECTRUMbusiness.industrymedicine.diseaseNeurology (clinical)businessCOLLECTIONEXPRESSION ANALYSISGene Deletion
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Amelioration of the abnormal phenotype of a new L1 syndrome mouse mutation with L1 mimetics

2021

L1 syndrome is a rare developmental disorder characterized by hydrocephalus of varying severity, intellectual deficits, spasticity of the legs, and adducted thumbs. Therapy is limited to symptomatic relief. Numerous gene mutations in the L1 cell adhesion molecule (L1CAM, hereafter abbreviated L1) were identified in L1 syndrome patients, and those affecting the extracellular domain of this transmembrane type 1 glycoprotein show the most severe phenotypes. Previously analyzed rodent models of the L1 syndrome focused on L1-deficient animals or mouse mutants with abrogated cell surface expression of L1, making it difficult to test L1 function-triggering mimetic compounds with potential therapeu…

Male0301 basic medicineToluidinesL1NeurogenesisCellNeural Cell Adhesion Molecule L1Gene mutationBiologyDuloxetine Hydrochloridemedicine.disease_causeBiochemistryCerebral VentriclesCorpus CallosumMice03 medical and health sciences0302 clinical medicineCerebellumIntellectual DisabilityGeneticsmedicineExtracellularAnimalsL1 syndromeMolecular BiologyCells CulturedNeuronsMutationSpastic Paraplegia HereditaryTrimebutineGenetic Diseases X-LinkedCell migrationSymptomatic reliefMice Inbred C57BLPhenotype030104 developmental biologymedicine.anatomical_structureMutationCancer researchPeptidomimeticsLocomotion030217 neurology & neurosurgeryBiotechnologyThe FASEB Journal
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Glial expression of Swiss cheese (SWS), the Drosophila orthologue of neuropathy target esterase (NTE), is required for neuronal ensheathment and func…

2016

ABSTRACT Mutations in Drosophila Swiss cheese (SWS) or its vertebrate orthologue neuropathy target esterase (NTE), respectively, cause progressive neuronal degeneration in Drosophila and mice and a complex syndrome in humans that includes mental retardation, spastic paraplegia and blindness. SWS and NTE are widely expressed in neurons but can also be found in glia; however, their function in glia has, until now, remained unknown. We have used a knockdown approach to specifically address SWS function in glia and to probe for resulting neuronal dysfunctions. This revealed that loss of SWS in pseudocartridge glia causes the formation of multi-layered glial whorls in the lamina cortex, the firs…

Medicine (miscellaneous)lcsh:MedicineAxonal degenerationSynaptic Transmission0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsNeurons0303 health sciencesGene knockdownCell Deathmusculoskeletal neural and ocular physiologyPhototaxisAnatomyCell biologymedicine.anatomical_structureDrosophila melanogasterPhospholipasesGene Knockdown TechniquesNeurogliaNeurogliaDrosophila Proteinpsychological phenomena and processesResearch Articlelcsh:RB1-214Programmed cell deathNeuriteNeuroscience (miscellaneous)Nerve Tissue ProteinsNeuropathy target esteraseNeurotransmissionBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesPNPLA6mental disordersNeuropilmedicineNeuriteslcsh:PathologyAnimalsPhospholipaseCell Shape030304 developmental biologySequence Homology Amino AcidSpastic paraplegialcsh:R302Reproducibility of ResultsEnsheathing gliabody regionsnervous systemVacuolesbiology.proteinCarboxylic Ester Hydrolases030217 neurology & neurosurgeryDisease Models & Mechanisms
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A total of 220 patients with autosomal dominant spastic paraplegia do not display mutations in the SLC33A1 gene (SPG42).

2010

The most frequent causes of autosomal dominant (AD) hereditary spastic paraplegias (HSP) (ADHSP) are mutations in the SPAST gene (SPG4 locus). However, roughly 60% of patients are negative for SPAST mutations, despite their family history being compatible with AD inheritance. A mutation in the gene for an acetyl-CoA transporter (SLC33A1) has recently been reported in one Chinese family to cause ADHSP-type SPG42. In this study, we screened 220 independent SPAST mutation-negative ADHSP samples for mutations in the SLC33A1 gene by high-resolution melting curve analysis. Conspicuous samples were validated by direct sequencing. Moreover, copy number variations affecting SLC33A1 were screened by …

GeneticsParaplegiamedicine.diagnostic_testgenetics [Membrane Transport Proteins]Hereditary spastic paraplegiaSLC33A1 protein humanShort ReportMembrane Transport ProteinsLocus (genetics)BiologyGene mutationmedicine.diseaseGene dosagegenetics [Paraplegia]MutationGeneticsmedicineHumansCopy-number variationddc:610Family historyGeneGenetics (clinical)Genetic testingGenes Dominant
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Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

2018

© 2018 Elsevier Inc.

MaleAls geneGenome-wide association studyFAMILIAL ALSALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS0302 clinical medicine80 and overPsychologyGWASKIF5AAetiologycargoAged 80 and over0303 health sciencesFrench ALS ConsortiumKinesinKINESIN HEAVY-CHAINCognitive Sciencesaxonal transportHumanHereditary spastic paraplegiaNeuroscience(all)Single-nucleotide polymorphismTARGETED DISRUPTIONArticle03 medical and health sciencesGeneticsHumansAmino Acid SequenceLoss functionAgedHEXANUCLEOTIDE REPEATNeuroscience (all)MUTATIONSAmyotrophic Lateral Sclerosis3112 Neurosciences1702 Cognitive Sciencemedicine.diseaseITALSGEN ConsortiumAnswer ALS Foundation030104 developmental biologyALS Sequencing ConsortiumHuman medicine1109 Neurosciences030217 neurology & neurosurgery0301 basic medicineALS; GWAS; KIF5A; WES; WGS; axonal transport; cargo[SDV]Life Sciences [q-bio]KinesinsNeurodegenerativeGenetic analysisGenomeAMYOTROPHIC-LATERAL-SCLEROSIS3124 Neurology and psychiatryCohort StudiesPathogenesisLoss of Function MutationMissense mutation2.1 Biological and endogenous factorsAmyotrophic lateral sclerosisNYGC ALS ConsortiumGeneticsGeneral NeuroscienceALS axonal transport cargo GWAS KIF5A WES WGSMiddle AgedPhenotypeSettore MED/26 - NEUROLOGIANeurologicalProject MinE ALS Sequencing ConsortiumKinesinWESFemaleAdultBiologyGENOTYPE IMPUTATIONALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Genome-Wide Association Study; Humans; Kinesin; Loss of Function Mutation; Male; Middle Aged; Young AdultNOYoung AdultRare DiseasesmedicineSLAGEN ConsortiumGene030304 developmental biologyClinical Research in ALS and Related Disorders for Therapeutic Development (CReATe) ConsortiumNeurology & NeurosurgeryHuman GenomeNeurosciencesAXONAL-TRANSPORTBrain DisordersALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS;Family memberDNA-DAMAGEMOTOR-NEURONS3111 BiomedicineCohort StudieALSGenomic Translation for ALS Care (GTAC) ConsortiumWGSAmyotrophic Lateral SclerosiGenome-Wide Association StudyALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Neuroscience (all)
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Identification of novel mutations in L1CAM gene by a DHPLC-based assay

2016

X-linked hydrocephalus, MASA syndrome, X-linked complicated Spastic Paraplegia Type I, and X-linked partial agenesis of the corpus callosum are rare diseases mainly affecting male population and broadly referred as L1 syndrome, caused by mutations in the L1CAM gene. In the present study 36 boys and a male fetus whose clinical features were consistent with L1 syndrome were analyzed by dHPLC assay and direct sequencing of L1CAM gene. Sequence analysis of the 14 different aberrant dHPLC elution profiles demonstrated that six of them were associated with already reported polymorphisms, four with previously described causative variants while the remaining four represented novel L1CAM mutations. …

0301 basic medicineGeneticsCRASH syndromeHydrocephaluSequence analysisSpastic paraplegiaMASA syndromeL1-diseaseBiologyCorpus callosummedicine.diseaseBiochemistryHuman geneticsHydrocephalus03 medical and health sciences030104 developmental biologyIntellectual disabilityGeneticsmedicineAdducted thumbDifferential diagnosisL1 syndromeMolecular BiologyGenes & Genomics
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Human SPG11 cerebral organoids reveal cortical neurogenesis impairment

2018

Abstract Spastic paraplegia gene 11(SPG11)-linked hereditary spastic paraplegia is a complex monogenic neurodegenerative disease that in addition to spastic paraplegia is characterized by childhood onset cognitive impairment, thin corpus callosum and enlarged ventricles. We have previously shown impaired proliferation of SPG11 neural progenitor cells (NPCs). For the delineation of potential defect in SPG11 brain development we employ 2D culture systems and 3D human brain organoids derived from SPG11 patients’ iPSC and controls. We reveal that an increased rate of asymmetric divisions of NPCs leads to proliferation defect, causing premature neurogenesis. Correspondingly, SPG11 organoids appe…

GenotypeHereditary spastic paraplegiaNeurogenesisFluorescent Antibody TechniqueBiology03 medical and health sciencesGlycogen Synthase Kinase 3GeneticsOrganoidmedicineSpasticHumansMolecular BiologyGenetics (clinical)Allelesbeta CateninCerebral Cortex0303 health sciences030305 genetics & heredityNeurogenesisProteinsGeneral MedicineHuman brainmedicine.diseaseNeural stem cellnervous system diseasesOrganoidsmedicine.anatomical_structurePhenotypeMutationGeneral ArticleDisease SusceptibilityParaplegiaCognition DisordersNeuroscienceNeural developmentBiomarkersHuman Molecular Genetics
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Frequency and phenotype of SPG11 and SPG15 in complicated hereditary spastic paraplegia

2009

Background: Hereditary spastic paraplegias (HSP) are clinically and genetically highly heterogeneous. Recently, two novel genes, SPG11 ( spatacsin ) and SPG15 ( spastizin ), associated with autosomal recessive HSP, were identified. Clinically, both are characterised by complicated HSP and a rather similar phenotype consisting of early onset spastic paraplegia, cognitive deficits, thin corpus callosum (TCC), peripheral neuropathy and mild cerebellar ataxia. Objective: To compare the frequency of SPG11 and SPG15 in patients with early onset complicated HSP and to further characterise the phenotype of SPG11 and SPG15. Results: A sample of 36 index patients with early onset complicated HSP and …

AdultMaleAdolescentHereditary spastic paraplegiaGenes RecessiveCompound heterozygosityCorpus callosumCorpus CallosumYoung AdultGene FrequencyIntellectual DisabilitySpasticHumansMedicineMutation frequencyAllele frequencyGenetic Association StudiesPolymorphism GeneticCerebellar ataxiaSpastic Paraplegia Hereditarybusiness.industryProteinsmedicine.diseasePhenotypePsychiatry and Mental healthPhenotypeMutationImmunologyFemaleSurgeryNeurology (clinical)medicine.symptomCarrier ProteinsbusinessNeuroscienceJournal of Neurology, Neurosurgery & Psychiatry
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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
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REEP1 mutation spectrum and genotype/phenotype correlation in hereditary spastic paraplegia type 31.

2008

Contains fulltext : 71291.pdf (Publisher’s version ) (Closed access) Mutations in the receptor expression enhancing protein 1 (REEP1) have recently been reported to cause autosomal dominant hereditary spastic paraplegia (HSP) type SPG31. In a large collaborative effort, we screened a sample of 535 unrelated HSP patients for REEP1 mutations and copy number variations. We identified 13 novel and 2 known REEP1 mutations in 16 familial and sporadic patients by direct sequencing analysis. Twelve out of 16 mutations were small insertions, deletions or splice site mutations. These changes would result in shifts of the open-reading-frame followed by premature termination of translation and haploins…

AdultMaleMutation rateAdolescentGenotypeHereditary spastic paraplegiaDNA Mutational AnalysisBiologymedicine.disease_causeArticleCognitive neurosciences [UMCN 3.2]Gene duplicationGenotypemedicinePerception and Action [DCN 1]HumansCopy-number variationAge of OnsetMutation frequencyChildAgedAged 80 and overGeneticsMutationHereditary cancer and cancer-related syndromes [ONCOL 1]Spastic Paraplegia HereditaryInfantMembrane Transport ProteinsMiddle Agedmedicine.diseasePedigreePhenotypeChild PreschoolMutationFemaleNeurology (clinical)HaploinsufficiencyFunctional Neurogenomics [DCN 2]
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