Search results for "Intellect"

showing 10 items of 642 documents

Variant recurrence in neurodevelopmental disorders: the use of publicly available genomic data identifies clinically relevant pathogenic missense var…

2019

Next-generation sequencing has revealed the major impact of de novo variants (DNVs) in developmental disorders (DD) such as intellectual disability, autism, and epilepsy. However, a substantial fraction of these predicted pathogenic DNVs remains challenging to distinguish from background DNVs, notably the missense variants acting via nonhaploinsufficient mechanisms on specific amino acid residues. We hypothesized that the detection of the same missense variation in at least two unrelated individuals presenting with a similar phenotype could be a powerful approach to reveal novel pathogenic variants. We looked for variations independently present in both our database of >1200 solo exomes and…

Male0301 basic medicineCandidate geneDevelopmental DisabilitiesMutation Missense030105 genetics & heredityBiology03 medical and health sciencesNeurodevelopmental disorderIntellectual DisabilityDatabases GeneticIntellectual disabilitymedicineHumansMissense mutationExomeGenetic Predisposition to DiseaseGenetic TestingAutistic DisorderGeneGenetics (clinical)Exome sequencingGeneticsComputational BiologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAmedicine.diseasePhenotype030104 developmental biologyNeurodevelopmental DisordersAutismFemaleTranscription FactorsGenetics in Medicine
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High Rate of Recurrent De Novo Mutations in Developmental and Epileptic Encephalopathies

2017

Item does not contain fulltext Developmental and epileptic encephalopathy (DEE) is a group of conditions characterized by the co-occurrence of epilepsy and intellectual disability (ID), typically with developmental plateauing or regression associated with frequent epileptiform activity. The cause of DEE remains unknown in the majority of cases. We performed whole-genome sequencing (WGS) in 197 individuals with unexplained DEE and pharmaco-resistant seizures and in their unaffected parents. We focused our attention on de novo mutations (DNMs) and identified candidate genes containing such variants. We sought to identify additional subjects with DNMs in these genes by performing targeted sequ…

Male0301 basic medicineCandidate genemedicine.medical_specialtymedical geneticsglycosylationNonsense mutationGenome-wide association studyGene mutationBiologySensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Articlesevere intellectual disability03 medical and health sciencesEpilepsy0302 clinical medicinechildrenRecurrenceSeizuresGenetic linkageIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyJournal ArticleGeneticsmedicineHumansChilddisordersGenetics (clinical)Genetic associationGeneticsBrain DiseasesdiseaseEpilepsycis-prenyltransferaseGenome Humanstructural basismedicine.diseasediphosphate synthase030104 developmental biologyChild PreschoolMutationMedical geneticsFemalenogo-b receptor030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenome-Wide Association StudyMeta-Analysis
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Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
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A novel mutation of WDR62 gene associated with severe phenotype including infantile spasm, microcephaly, and intellectual disability

2017

Abstract The autosomal recessive form of primary microcephaly (MCPH) is a rare disorder characterized by head circumference of at least 3 standard deviation below the mean. The MCPH exhibits genetic heterogeneity with thirteen loci (MCPH1-MCPH13) identified, and associated with variable degree of intellectual disability. It has been reported that WDR62 is the second causative gene of autosomal recessive microcephaly (MCPH2) playing a significant role in spindle formation and the proliferation of neuronal progenitor cells. We report a clinical feature, electroclinical findings, and clinical course of a patient with a severe phenotype of MCPH2 including microcephaly, refractory infantile spas…

Male0301 basic medicineMicrocephalyAdolescentMutation MissenseIntellectual disabilityCell Cycle ProteinsNerve Tissue ProteinsGenetic analysisReceptors G-Protein-CoupledConsanguinity03 medical and health sciences0302 clinical medicineDevelopmental NeuroscienceSettore M-PSI/08 - Psicologia ClinicaIntellectual disabilityHumansMedicineMissense mutationGeneWDR62GeneticsMCPHEpilepsybusiness.industryGenetic heterogeneityInfantGeneral MedicineInfantile Spasmmedicine.diseaseSettore MED/39 - Neuropsichiatria InfantilePedigreePhenotype030104 developmental biologyGPR56MutationPediatrics Perinatology and Child HealthMicrocephalyInfantile spasmNeurology (clinical)businessSpasms Infantile030217 neurology & neurosurgeryBrain and Development
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A Recurrent De Novo PACS2 Heterozygous Missense Variant Causes Neonatal-Onset Developmental Epileptic Encephalopathy, Facial Dysmorphism, and Cerebel…

2018

International audience; Developmental and epileptic encephalopathies (DEEs) represent a large clinical and genetic heterogeneous group of neurodevelopmental diseases. The identification of pathogenic genetic variants in DEEs remains crucial for deciphering this complex group and for accurately caring for affected individuals (clinical diagnosis, genetic counseling, impacting medical, precision therapy, clinical trials, etc.). Whole-exome sequencing and intensive data sharing identified a recurrent de novo PACS2 heterozygous missense variant in 14 unrelated individuals. Their phenotype was characterized by epilepsy, global developmental delay with or without autism, common cerebellar dysgene…

Male0301 basic medicinePathologyPACS-2Vesicular Transport ProteinsPHENOTYPEBioinformaticsDISEASESensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Epilepsy0302 clinical medicineMissense mutationGlobal developmental delayAge of OnsetChildGenetics (clinical)Epileptic encephalopathyAPOPTOSIS3. Good healthcerebellar dysgenesisMutation Missense/geneticsintellectual disabilityChild PreschoolEpilepsy GeneralizedFemalePACS2CLINICAL EPILEPSYmedicine.medical_specialtyHeterozygoteGeneralized/geneticsPROTEINSGenetic counselingMutation MissenseMissense/geneticsNeonatal onsetBiologyDIAGNOSISVesicular Transport Proteins/geneticsFacial dysmorphism03 medical and health sciencesDysgenesisAll institutes and research themes of the Radboud University Medical CenterCerebellar DiseasesReportMENDELIAN DISORDERSGeneticsmedicineHumansGeneralized epilepsyPreschoolNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cerebellar Diseases/geneticsbusiness.industryMUTATIONSInfant NewbornCorrectionInfantFaciesNewbornmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationepilepsyAutismbusinessEpilepsy Generalized/genetics030217 neurology & neurosurgery
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Application of whole-exome sequencing to unravel the molecular basis of undiagnosed syndromic congenital neutropenia with intellectual disability

2016

International audience; Neutropenia can be qualified as congenital when of neonatal onset or when associated with extra-hematopoietic manifestations. Overall, 30% of patients with congenital neutropenia (CN) remain without a molecular diagnosis after a multidisciplinary consultation and tedious diagnostic strategy. In the rare situations when neutropenia is identified and associated with intellectual disability (ID), there are few diagnostic hypotheses to test. This retrospective multicenter study reports on a clinically heterogeneous cohort of 10 unrelated patients with CN associated with ID and no molecular diagnosis prior to whole-exome sequencing (WES). WES provided a diagnostic yield o…

Male0301 basic medicinePediatricsmedicine.medical_specialtyNeutropeniaAdolescentNeonatal onsetNeutropenia03 medical and health sciences0302 clinical medicinecongenital neutropenia[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual DisabilityIntellectual disabilityGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansExomeChildCongenital NeutropeniaGenetic Association StudiesGenetics (clinical)Exome sequencingRetrospective Studiesbusiness.industryHigh-Throughput Nucleotide SequencingInfantSyndromemedicine.disease3. Good healthPhenotype030104 developmental biologyCHD2Child Preschool030220 oncology & carcinogenesisCohortEtiologyFemalebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBiomarkersAmerican Journal of Medical Genetics Part A
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Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome

2020

Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an impri…

Male0301 basic medicinePotassium Channels[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyGeneral Physics and AstronomyDiseasePhenylenediamines[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCraniofacial AbnormalitiesHistonesMice0302 clinical medicineIntellectual disabilityImprinting (psychology)lcsh:ScienceMice KnockoutGeneticsMultidisciplinaryBehavior AnimalbiologyNeurodevelopmental disordersDevelopmental disordersQBrainPhenotypeUp-RegulationPhenotypeHistoneGene Knockdown TechniquesBenzamidesMuscle HypotoniaFemaleLocus CoeruleusEpigeneticsScienceArticleGeneral Biochemistry Genetics and Molecular BiologyGenomic Imprinting03 medical and health sciencesDevelopmental disorders ; Neurodevelopmental disorders ; EpigeneticsIntellectual DisabilitymedicineAnimalsHumansddc:610AlleleGene[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Chemistrymedicine.diseaseHistone Deacetylase InhibitorsMice Inbred C57BLDisease Models Animal030104 developmental biologyAcetylationMutationbiology.proteinlcsh:Q030217 neurology & neurosurgery
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A new family with an SLC9A6 mutation expanding the phenotypic spectrum of Christianson syndrome

2016

Using targeted next generation sequencing, we have identified a splicing mutation (c.526-9_526-5del) in the SLC9A6 gene in a 9-year-old boy with mild intellectual disability (ID), microcephaly, and social interaction disabilities. This intronic microdeletion leads to the skipping of exon 3 and to an in-frame deletion of 26 amino acids in the TM4 domain. It segregates with cognitive impairment or learning difficulties in other members of the family. Mutations in SLC9A6 have been reported in X-linked Christianson syndrome associating severe to profound intellectual deficiency and an Angelman-like phenotype with microcephaly, absent speech, ataxia with progressive cerebellar atrophy, ophthalmo…

Male0301 basic medicineProbandMicrocephalyDNA Mutational Analysisx-chromosome inactivationSLC9A6Gene mutationexchangerEpilepsyOcular Motility Disorders0302 clinical medicineangelman-syndromeX Chromosome InactivationIntellectual disabilitymicrocephalyChild10. No inequalityGenetics (clinical)Sequence DeletionGeneticsBrainGenetic Diseases X-LinkedtoolMagnetic Resonance ImagingPedigree3. Good healthPhenotypeFemaleCerebellar atrophyChristianson syndromemedicine.symptomAdultHeterozygoteSodium-Hydrogen ExchangersAtaxiaAdolescentlearning disabilities linked mental-retardation03 medical and health sciencescerebellar atrophyIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyAngelman syndromeGeneticsmedicineHumansFamilygeneGenetic Association Studiesbusiness.industryFaciesmedicine.disease030104 developmental biologysplicing signalsMutationepilepsyAtaxiaRNA Splice Sitesbusiness030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Skraban‐Deardorff syndrome: Six new cases of WDR 26 ‐related disease and expansion of the clinical phenotype

2021

International audience; Skraban-Deardorff syndrome (a disease related to variations in the WDR26 gene; OMIM #617616) was first described in a cohort of 15 individuals in 2017. The syndrome comprises intellectual deficiency, severe speech impairment, ataxic gait, seizures, mild hypotonia with feeding difficulties during infancy, and dysmorphic features. Here, we report on six novel heterozygous de novo pathogenic variants in WDR26 in six probands. The patients’ phenotypes were consistent with original publication. One patient displayed marked hypotonia with an abnormal muscle biopsy; this finding warrants further investigation. Gait must be closely monitored, in order to highlight any muscul…

Male0301 basic medicineProbandPediatricsmedicine.medical_specialtyAdolescent[SDV]Life Sciences [q-bio]Developmental DisabilitiesSkraban-Deardorff syndromeDisease030105 genetics & heredityYoung Adult03 medical and health sciencesIntellectual disabilityGeneticsmedicineWDR26HumansAbnormalities MultiplehypotoniaAtaxic GaitChildGenetics (clinical)Adaptor Proteins Signal Transducing[SDV.GEN]Life Sciences [q-bio]/GeneticsMuscle biopsymedicine.diagnostic_testbusiness.industryInfantSyndromemedicine.diseaseGaitHypotonia3. Good health[SDV] Life Sciences [q-bio]Phenotype030104 developmental biologyspeech therapyintellectual disabilityChild PreschoolMutationCohortlanguage development disordersFemalemedicine.symptombusinessClinical Genetics
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Generation of an iPSC line (UNINAi001-A) from a girl with neonatal-onset epilepsy and non-syndromic intellectual disability carrying the homozygous K…

2021

Abstract Heterozygous variants in the KCNQ3 gene cause epileptic and/or developmental disorders of varying severity. Here we describe the generation of induced pluripotent stem cells (iPSCs) from a 9-year-old girl with pharmacodependent neonatal-onset epilepsy and intellectual disability who carry a homozygous single-base duplication in exon 12 of KCNQ3 (NM_004519.3: KCNQ3 c.1599dup; KCNQ3 p.PHE534ILEfs*15), and from a non-carrier brother of the proband. For iPSC generation, non-integrating episomal plasmid vectors were used to transfect fibroblasts isolated from skin biopsies. The obtained iPSC lines had a normal karyotype, showed embryonic stem cell-like morphology, expressed pluripotency…

Male0301 basic medicineProbandQH301-705.5Induced Pluripotent Stem CellsBiology03 medical and health sciencesEpilepsyExon0302 clinical medicineIntellectual DisabilityGene duplicationIntellectual disabilitymedicineHumansBiology (General)ChildInduced pluripotent stem cellEpilepsySiblingsHomozygoteCell DifferentiationKaryotypeCell BiologyGeneral Medicinemedicine.diseaseEmbryonic stem cell030104 developmental biologyCancer researchFemale030217 neurology & neurosurgeryDevelopmental Biology
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