Search results for "developmental disorders"

showing 10 items of 87 documents

DLG4-related synaptopathy: a new rare brain disorder

2021

Contains fulltext : 245031.pdf (Publisher’s version ) (Closed access) PURPOSE: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. METHODS: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. RESULTS: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit-hyp…

0301 basic medicineAutism Spectrum Disorder[SDV]Life Sciences [q-bio]030105 genetics & heredityBiology03 medical and health sciencesIntellectual DisabilityIntellectual disabilitymedicineMissense mutationHumansGlobal developmental delayExomeGenetics (clinical)GeneticsBrain DiseasesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Brainmedicine.disease030104 developmental biologyPhenotypeRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Autism spectrum disorderNeurodevelopmental DisordersSynaptopathyDLG4Postsynaptic densityDisks Large Homolog 4 Protein
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RBFOX1, encoding a splicing regulator, is a candidate gene for aggressive behavior

2020

The RBFOX1 gene (or A2BP1) encodes a splicing factor important for neuronal development that has been related to autism spectrum disorder and other neurodevelopmental phenotypes. Evidence from complementary sources suggests that this gene contributes to aggressive behavior. Suggestive associations with RBFOX1 have been identified in genome-wide association studies (GWAS) of anger, conduct disorder, and aggressive behavior. Nominal association signals in RBFOX1 were also found in an epigenome-wide association study (EWAS) of aggressive behavior. Also, variants in this gene affect temporal lobe volume, a brain area that is altered in several aggression-related phenotypes. In animals, this gen…

0301 basic medicineCandidate geneNeuroimagingRBFOX1Genome-wide association studyBiologyEpigenesis GeneticA2BP103 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineGeneticsmedicineAnimalsHumansPharmacology (medical)TranscriptomicsRBFOX1Genetic Association StudiesBiological PsychiatryRegulator genePharmacologyGeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]AggressionGenetic Variationmedicine.diseasePhenotypeAnimal modelsAggressionPsychiatry and Mental health030104 developmental biologyNeurologyAutism spectrum disorderEpigeneticsRBFOX1 GeneRNA Splicing FactorsNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryGenome-Wide Association Study
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SLC20A1 Is Involved in Urinary Tract and Urorectal Development

2020

Previous studies in developing Xenopus and zebrafish reported that the phosphate transporter slc20a1a is expressed in pronephric kidneys. The recent identification of SLC20A1 as a monoallelic candidate gene for cloacal exstrophy further suggests its involvement in the urinary tract and urorectal development. However, little is known of the functional role of SLC20A1 in urinary tract development. Here, we investigated this using morpholino oligonucleotide knockdown of the zebrafish ortholog slc20a1a. This caused kidney cysts and malformations of the cloaca. Moreover, in morphants we demonstrated dysfunctional voiding and hindgut opening defects mimicking imperforate anus in human cloacal exs…

0301 basic medicineCandidate genePathologyMorpholinoPediatricsEmbryonalentwicklungBlasenekstrophieBladder exstrophyZebrabärbling0302 clinical medicinebladder exstrophy-epispadias complex; CAKUT; cloacal malformation; functional genetics; kidney formation; SLC20A1; urinary tract development; zebrafish developmentbladder exstrophy-epispadias complexUrinary tract; Growth and developmentZebrafishlcsh:QH301-705.5ZebrafishNiereOriginal Researchcloacal malformationKidney; EmbryologyPediatrikzebrafish developmentKidney; Growth and developmentReconstructive and regenerative medicine Radboud Institute for Molecular Life Sciences [Radboudumc 10]030220 oncology & carcinogenesisembryonic structuresfunctional geneticsmedicine.symptomSLC20A1medicine.medical_specialtyEpispadiasanimal structuresUrinary systemBiologyKidney cystsCell and Developmental Biology03 medical and health sciencesAll institutes and research themes of the Radboud University Medical Centermedicineddc:610CAKUTNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cloaca; Abnormalitieskidney formationCell Biologymedicine.diseaseCloacal exstrophybiology.organism_classificationurinary tract developmentReconstructive and regenerative medicine Radboud Institute for Health Sciences [Radboudumc 10]Bladder exstrophy030104 developmental biologyCloaca (embryology)lcsh:Biology (General)Developmental BiologyFrontiers in Cell and Developmental Biology
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Update on oral-facial-digital syndromes (OFDS)

2016

Oral-facial-digital syndromes (OFDS) represent a heterogeneous group of rare developmental disorders affecting the mouth, the face and the digits. Additional signs may involve brain, kidneys and other organs thus better defining the different clinical subtypes. With the exception of OFD types I and VIII, which are X-linked, the majority of OFDS is transmitted as an autosomal recessive syndrome. A number of genes have already found to be mutated in OFDS and most of the encoded proteins are predicted or proven to be involved in primary cilia/basal body function. Preliminary data indicate a physical interaction among some of those proteins and future studies will clarify whether all OFDS prote…

0301 basic medicineGeneticsCiliumOral facial digitalDevelopmental disorderDevelopmental disordersCell BiologyReviewBiologyBioinformaticsmedicine.diseasePhenotypeCiliopathiesHuman geneticsJoubert syndrome3. Good health03 medical and health sciences030104 developmental biologymedicineOFDSCiliaMeckel syndromeGene[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Influence of gut microbiota on neuropsychiatric disorders

2017

The last decade has witnessed a growing appreciation of the fundamental role played by an early assembly of a diverse and balanced gut microbiota and its subsequent maintenance for future health of the host. Gut microbiota is currently viewed as a key regulator of a fluent bidirectional dialogue between the gut and the brain (gut-brain axis). A number of preclinical studies have suggested that the microbiota and its genome (microbiome) may play a key role in neurodevelopmental and neurodegenerative disorders. Furthermore, alterations in the gut microbiota composition in humans have also been linked to a variety of neuropsychiatric conditions, including depression, autism and Parkinson’s dis…

0301 basic medicineHypothalamo-Hypophyseal SystemGut–brain axisPituitary-Adrenal SystemDiseaseGut floraBioinformaticsdigestive systemEpigenesis Genetic03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansBrain-gut axisMicrobiomePsychiatric conditionsbiologyMicrobiotaGastrointestinal MicrobiomeGastroenterologyBrainNeurodegenerative DiseasesMinireviewsGeneral MedicineDNA MethylationFecal Microbiota TransplantationMental illnessmedicine.diseasebiology.organism_classificationGastrointestinal MicrobiomeTransplantationDisease Models Animal030104 developmental biologyNeurodevelopmental DisordersDysbiosisMental healthMicrobiomeDysbiosisStress Psychological030217 neurology & neurosurgeryWorld Journal of Gastroenterology
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Loss-of-function and missense variants in NSD2 cause decreased methylation activity and are associated with a distinct developmental phenotype

2021

Purpose Despite a few recent reports of patients harboring truncating variants in NSD2, a gene considered critical for the Wolf–Hirschhorn syndrome (WHS) phenotype, the clinical spectrum associated with NSD2 pathogenic variants remains poorly understood. Methods We collected a comprehensive series of 18 unpublished patients carrying heterozygous missense, elongating, or truncating NSD2 variants; compared their clinical data to the typical WHS phenotype after pooling them with ten previously described patients; and assessed the underlying molecular mechanism by structural modeling and measuring methylation activity in vitro. Results The core NSD2-associated phenotype includes mostly mild dev…

0301 basic medicineIn silicoBiologyArticleREGION03 medical and health sciencesROGERS-DANKS-SYNDROME0302 clinical medicineMissense mutationHISTONE H3GeneGenetics (clinical)Loss functionGeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]DELETIONDEFECTSMethylationPhenotypeLYSINE 36030104 developmental biologyMolecular mechanismWOLF-HIRSCHHORN-SYNDROME030217 neurology & neurosurgeryFunction (biology)Rare cancers Radboud Institute for Health Sciences [Radboudumc 9]Genetics in Medicine
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De Novo and Inherited Pathogenic Variants in KDM3B Cause Intellectual Disability, Short Stature, and Facial Dysmorphism

2019

Contains fulltext : 202646.pdf (Publisher’s version ) (Open Access) By using exome sequencing and a gene matching approach, we identified de novo and inherited pathogenic variants in KDM3B in 14 unrelated individuals and three affected parents with varying degrees of intellectual disability (ID) or developmental delay (DD) and short stature. The individuals share additional phenotypic features that include feeding difficulties in infancy, joint hypermobility, and characteristic facial features such as a wide mouth, a pointed chin, long ears, and a low columella. Notably, two individuals developed cancer, acute myeloid leukemia and Hodgkin lymphoma, in childhood. KDM3B encodes for a histone …

0301 basic medicineMaleJumonji Domain-Containing Histone DemethylasesDevelopmental DisabilitiesWEAVER SYNDROMEPROTEINHaploinsufficiencyCraniofacial AbnormalitiesHistones0302 clinical medicineIntellectual disabilityTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Missense mutationDEMETHYLASE KDM3BExomeChildGenetics (clinical)Exome sequencingGeneticsRUBINSTEIN-TAYBI SYNDROMEMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Phenotype030220 oncology & carcinogenesisFemalemedicine.symptomHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Joint hypermobilityGENETICSJMJD1CMutation MissenseDwarfismBiologyShort statureKdm3b ; Cancer Predisposition ; Developmental Delay ; Facial Recognition ; Intellectual Disability ; Leukemia ; Lymphoma ; Short Stature03 medical and health sciencesReportIntellectual DisabilitymedicineHumansMYELOID-LEUKEMIAGenetic Association StudiesGerm-Line MutationWeaver syndromeNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Rubinstein–Taybi syndromeMUTATIONSDELETIONGenetic Variationmedicine.diseaseBody HeightMusculoskeletal AbnormalitiesINDIVIDUALS030104 developmental biologyFaceNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]American 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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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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