Search results for "neurodevelopment"

showing 10 items of 140 documents

Heterozygous Variants in KDM4B Lead to Global Developmental Delay and Neuroanatomical Defects

2020

International audience; KDM4B is a lysine-specific demethylase with a preferential activity on H3K9 tri/di-methylation (H3K9me3/2)-modified histones. H3K9 tri/di-demethylation is an important epigenetic mechanism responsible for silencing of gene expression in animal development and cancer. However, the role of KDM4B on human development is still poorly characterized. Through international data sharing, we gathered a cohort of nine individuals with mono-allelic de novo or inherited variants in KDM4B. All individuals presented with dysmorphic features and global developmental delay (GDD) with language and motor skills most affected. Three individuals had a history of seizures, and four had a…

0301 basic medicineMaleJumonji Domain-Containing Histone Demethylases[SDV]Life Sciences [q-bio]Developmental DisabilitiesCorpus callosumHippocampusEpigenesis GeneticHistonesMice0302 clinical medicineNeurodevelopmental disorderPolymicrogyriaGlobal developmental delayAgenesis of the corpus callosumGenetics (clinical)BrainMagnetic Resonance Imaging[SDV] Life Sciences [q-bio]intellectual disabilityBrain sizeFemaledysmorphic hippocampiSignal TransductionHeterozygoteheterozygous variantglobal developmental delayBiologyNervous System MalformationsMethylation03 medical and health sciencesSeizuresReportKDM4BGeneticsmedicineAnimalsHumansneurodevelopmental disorder.Dentate gyrusGenetic VariationJMJD2Bmedicine.diseaseneurodevelopmental disorder030104 developmental biologyagenesis of the corpus callosumNeuroscienceProtein Processing Post-Translational030217 neurology & neurosurgeryVentriculomegalyAmerican journal of human genetics
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Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Am J Hum Genet

2019

ZMIZ1 is a coactivator of several transcription factors, including p53, the androgen receptor, and NOTCH1. Here, we report 19 subjects with intellectual disability and developmental delay carrying variants in ZMIZ1. The associated features include growth failure, feeding difficulties, microcephaly, facial dysmorphism, and various other congenital malformations. Of these 19, 14 unrelated subjects carried de novo heterozygous single-nucleotide variants (SNVs) or single-base insertions/deletions, 3 siblings harbored a heterozygous single-base insertion, and 2 subjects had a balanced translocation disrupting ZMIZ1 or involving a regulatory region of ZMIZ1. In total, we identified 13 point mutat…

0301 basic medicineMaleMicrocephaly[SDV]Life Sciences [q-bio]Developmental DisabilitiesAucunBiology030226 pharmacology & pharmacyTransactivation03 medical and health sciencesMiceNeurodevelopmental disorder0302 clinical medicineReportIntellectual DisabilityCoactivatormedicineGeneticsAnimalsHumansPoint MutationAlleleChildExomeGenetics (clinical)Alleles030304 developmental biologyGenetics0303 health sciencesPoint mutationCorrectionInfantSyndromemedicine.diseaseAndrogen receptor030104 developmental biologyChild PreschoolFemale030217 neurology & neurosurgeryTranscription Factors
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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A Genome-Wide Association Meta-Analysis of Attention-Deficit/Hyperactivity Disorder Symptoms in Population-Based Pediatric Cohorts

2016

OBJECTIVE: The aims of this study were to elucidate the influence of common genetic variants on childhood attention-deficit/hyperactivity disorder (ADHD) symptoms, to identify genetic variants that explain its high heritability, and to investigate the genetic overlap of ADHD symptom scores with ADHD diagnosis. METHOD: Within the EArly Genetics and Lifecourse Epidemiology (EAGLE) consortium, genome-wide single nucleotide polymorphisms (SNPs) and ADHD symptom scores were available for 17,666 children (<13 years of age) from nine population-based cohorts. SNP-based heritability was estimated in data from the three largest cohorts. Meta-analysis based on genome-wide association (GWA) analyses w…

0301 basic medicineMaleNetherlands Twin Register (NTR)attention problemsPopulation/methodsCHILDHOODAdhd Symptoms ; Gwa ; Snp Heritability ; Attention Problems ; Meta-analysisGenome-wide association studyCHILDRENCohort Studies0302 clinical medicineDevelopmental and Educational PsychologyGENETIC INFLUENCESNETHERLANDS TWIN REGISTERChildGeneticsRISKeducation.field_of_studyGenetics Population/methods3. Good healthPsychiatry and Mental healthPERSONALITY CONSORTIUM/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemalePsychologyAttention Deficit Disorder with Hyperactivity/geneticsAdolescentDEFICIT HYPERACTIVITY DISORDERPopulationSingle-nucleotide polymorphismGWAPROFILEGenetic correlationADHD symptomsArticle150 000 MR Techniques in Brain FunctionSNP heritabilityBEHAVIOR PROBLEMS03 medical and health sciencesSDG 3 - Good Health and Well-beingmedicine/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_GeneticsSNPAttention deficit hyperactivity disorderADHDHumanseducationGenetic associationNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Heritabilitymedicine.diseasemeta-analysis030104 developmental biologyGenetics PopulationTrastorn per dèficit d'atenció amb hiperactivitatAttention Deficit Disorder with HyperactivityCase-Control Studies030217 neurology & neurosurgeryGenèticaGenome-Wide Association Study
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Pathogenic DDX3X Mutations Impair RNA Metabolism and Neurogenesis during Fetal Cortical Development.

2020

Summary De novo germline mutations in the RNA helicase DDX3X account for 1%–3% of unexplained intellectual disability (ID) cases in females and are associated with autism, brain malformations, and epilepsy. Yet, the developmental and molecular mechanisms by which DDX3X mutations impair brain function are unknown. Here, we use human and mouse genetics and cell biological and biochemical approaches to elucidate mechanisms by which pathogenic DDX3X variants disrupt brain development. We report the largest clinical cohort to date with DDX3X mutations (n = 107), demonstrating a striking correlation between recurrent dominant missense mutations, polymicrogyria, and the most severe clinical outcom…

0301 basic medicineMaleNeurogenesisMutation MissenseBiologyPathogenesisDEAD-box RNA Helicases03 medical and health sciencesMice0302 clinical medicineGermline mutationStress granuleCell Line TumorPolymicrogyriamedicineMissense mutationAnimalsHumansCells CulturedGeneticsCerebral CortexGeneral NeuroscienceNeurogenesismedicine.diseaseRNA Helicase AMice Inbred C57BL030104 developmental biologyNeurodevelopmental DisordersRNAFemaleDDX3X030217 neurology & neurosurgeryNeuron
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GLRB allelic variation associated with agoraphobic cognitions, increased startle response and fear network activation: a potential neurogenetic pathw…

2017

Contains fulltext : 177350.pdf (Publisher’s version ) (Closed access) The molecular genetics of panic disorder (PD) with and without agoraphobia (AG) are still largely unknown and progress is hampered by small sample sizes. We therefore performed a genome-wide association study with a dimensional, PD/AG-related anxiety phenotype based on the Agoraphobia Cognition Questionnaire (ACQ) in a sample of 1370 healthy German volunteers of the CRC TRR58 MEGA study wave 1. A genome-wide significant association was found between ACQ and single non-coding nucleotide variants of the GLRB gene (rs78726293, P=3.3 x 10-8; rs191260602, P=3.9 x 10-8). We followed up on this finding in a larger dimensional AC…

0301 basic medicineMaleStartle responseReflex StartleQH301 BiologyGenome-wide association studyGene mutationAnxiety0302 clinical medicineCognitionReceptors GlycineGene FrequencyGermanyGWASHyperekplexiaGeneticsPanic disordermedicine.diagnostic_testStartleBrainFearGLRBAnxiety DisordersPsychiatry and Mental healthSchizophreniaUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Panic DisorderFemalemedicine.symptomPsychologyBDCRC0321 Neuroscience. Biological psychiatry. NeuropsychiatryClinical psychologyAdultGenotypeNDASQH426 Genetics03 medical and health sciencesCellular and Molecular NeuroscienceQH301Fear networkSpastic mousemedicineHumansGenetic Predisposition to DiseaseMolecular BiologyQH426AgoraphobiaAllelesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Panic disorderOther Research Radboud Institute for Health Sciences [Radboudumc 0]medicine.diseaseStartle reaction030104 developmental biologyMCPCase-Control StudiesMutationRC0321030217 neurology & neurosurgeryAgoraphobiaGenome-Wide Association StudyMolecular psychiatry
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The broad phenotypic spectrum of PPP2R1A -related neurodevelopmental disorders correlates with the degree of biochemical dysfunction

2021

PURPOSE: Neurodevelopmental disorders (NDD) caused by protein phosphatase 2A (PP2A) dysfunction have mainly been associated with de novo variants in PPP2R5D and PPP2CA, and more rarely in PPP2R1A. Here, we aimed to better understand the latter by characterizing 30 individuals with de novo and often recurrent variants in this PP2A scaffolding Aα subunit. METHODS: Most cases were identified through routine clinical diagnostics. Variants were biochemically characterized for phosphatase activity and interaction with other PP2A subunits. RESULTS: We describe 30 individuals with 16 different variants in PPP2R1A, 21 of whom had variants not previously reported. The severity of developmental delay …

0301 basic medicineMicrocephaly[SDV]Life Sciences [q-bio]Intellectual disability030105 genetics & heredityBioinformaticsEpilepsyNeurodevelopmental disorderIntellectual disabilityCOREProtein Phosphatase 2SPECIFICITYGenetics (clinical)PROTEIN PHOSPHATASE 2APhenotypeHypotoniaFAMILY3. Good healthPP2A[SDV] Life Sciences [q-bio]PPP2R1APPP2R5DINSIGHTSintellectual disabilityMicrocephalyMuscle Hypotoniamedicine.symptomLanguage delay[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsArticle03 medical and health sciencesNeurodevelopmental disorder[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpilepsybusiness.industryMacrocephalyDEPHOSPHORYLATIONmedicine.diseaseneurodevelopmental disorder030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNeurodevelopmental DisordersSUBUNITepilepsyHuman medicineTAUbusinessTranscription Factors
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Beyond protein-coding genes

2019

A long non-coding RNA called lnc-NR2F1 regulates several neuronal genes, including some involved in autism and intellectual disabilities.

0301 basic medicineMouseQH301-705.5ScienceautismGenomicsmacromolecular substancesComputational biologyBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntellectual Disabilitymental disordersgenomicsneuronal developmentmedicineAnimalsHumansAutistic DisorderBiology (General)GeneNeuronsProtein codingRegulation of gene expressionCOUP Transcription Factor Ilong non-coding RNAGeneral Immunology and MicrobiologyGeneral NeuroscienceQRProteinsRNAGenetics and GenomicsGeneral Medicinemedicine.diseaseLong non-coding RNA030104 developmental biologynervous systemNeurodevelopmental DisordersMedicineAutismRNA Long Noncodingintellectual disabilitiesInsightgene regulation030217 neurology & neurosurgeryHumaneLife
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Functional analysis of TLK2 variants and their proximal interactomes implicates impaired kinase activity and chromatin maintenance defects in their p…

2020

IntroductionThe Tousled-like kinases 1 and 2 (TLK1 and TLK2) are involved in many fundamental processes, including DNA replication, cell cycle checkpoint recovery and chromatin remodelling. Mutations in TLK2 were recently associated with ‘Mental Retardation Autosomal Dominant 57’ (MRD57, MIM# 618050), a neurodevelopmental disorder characterised by a highly variable phenotype, including mild-to-moderate intellectual disability, behavioural abnormalities, facial dysmorphisms, microcephaly, epilepsy and skeletal anomalies.MethodsWe re-evaluate whole exome sequencing and array-CGH data from a large cohort of patients affected by neurodevelopmental disorders. Using spatial proteomics (BioID) and…

0301 basic medicineNeurobiologia del desenvolupamentMicrocephalymissenseMolecular biologyBiologymedicine.disease_causemedicalloss of function mutation03 medical and health sciencesmutation.0302 clinical medicineNeurodevelopmental disordermedicineChromatin maintenanceMissense mutationmolecular biologygeneticsDevelopmental neurobiologyKinase activitygenetic research; genetics; loss of function mutation; medical; missense; molecular biology; mutationGenetics (clinical)Exome sequencingBiologia molecularGeneticsMutationgenetic researchmedicine.diseaseChromatin030104 developmental biologymutationgenetic030217 neurology & neurosurgery
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