Search results for "NeuroD"

showing 10 items of 604 documents

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
researchProduct

Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.

2017

Background Adult neurogenesis persists through life at least in classic neurogenic niches. Neurogenesis has been previously described as reduced in neurodegenerative diseases. There is not much knowledge about is adult neurogenesis is or not modified in amyotrophy lateral sclerosis (ALS). All previous publications has studied the ALS SOD1 (superoxide dismutase) transgenic mouse model. The purpose of this study is to examine the process of adult neurogenesis in classic niches (subventricular zone [SVZ] and subgranular zone [SGZ] of the dentate gyrus) in patients with amyotrophic lateral sclerosis (ALS), both with (ALS-FTD) and without associated frontotemporal dementia (FTD). Methods We stud…

0301 basic medicineMalePathologymedicine.medical_specialtyDoublecortin ProteinTDP-43NeurogenesisSOD1Subventricular zoneAdult neurogenesislcsh:RC346-429Subgranular zone03 medical and health sciences0302 clinical medicineNeuroblastNeural Stem CellsLateral VentriclesMedicineHumansAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemAgedAged 80 and overbusiness.industryDentate gyrusNeurogenesisAmyotrophic Lateral SclerosisNeurodegenerative diseasesBrainGeneral MedicineMiddle Agedmedicine.diseaseNeural stem cellnervous system diseases030104 developmental biologymedicine.anatomical_structurenervous systemFrontotemporal DementiaFemaleNeurology (clinical)business030217 neurology & neurosurgeryResearch ArticleBMC neurology
researchProduct

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
researchProduct

Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
researchProduct

Genetic and constitutional factors are major contributors to substantia nigra hyperechogenicity

2017

9 páginas, 2 figuras, 4 tablas

0301 basic medicineMalemedicine.medical_specialtyMovement disordersScienceSubstantia nigraDiseaseComorbidityArticle03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansGenetic Predisposition to DiseaseFamily historyAmyotrophic lateral sclerosisPsychiatryGenetic Association StudiesGenetic testingAgedUltrasonographyMultidisciplinarymedicine.diagnostic_testbusiness.industryQCase-control studyRNeurodegenerative DiseasesMiddle Agedmedicine.diseaseComorbiditySubstantia Nigra030104 developmental biologyCase-Control StudiesMutationMedicineFemalemedicine.symptombusiness030217 neurology & neurosurgeryBiomarkers
researchProduct

Drosophila melanogaster Models of Metal-Related Human Diseases and Metal Toxicity

2017

Iron, copper and zinc are transition metals essential for life because they are required in a multitude of biological processes. Organisms have evolved to acquire metals from nutrition and to maintain adequate levels of each metal to avoid damaging effects associated with its deficiency, excess or misplacement. Interestingly, the main components of metal homeostatic pathways are conserved, with many orthologues of the human metal-related genes having been identified and characterized in Drosophila melanogaster. Drosophila has gained appreciation as a useful model for studying human diseases, including those caused by mutations in pathways controlling cellular metal homeostasis. Flies have m…

0301 basic medicineMetal toxicityDiseaseComputational biologyReviewCatalysisInorganic Chemistrylcsh:Chemistry03 medical and health sciencesironATP7Metals HeavyMetalloproteinsmedicineAnimalsDrosophila ProteinsToxicologiaPhysical and Theoretical ChemistryMolecular BiologyGeneDrosophilalcsh:QH301-705.5SpectroscopyOrganismMetal Metabolism Inborn ErrorsMetal metabolismfrataxinbiologyEcologyOrganic ChemistryNeurodegenerationzincneurodegenerationGeneral Medicinemedicine.diseasebiology.organism_classificationdZip99CComputer Science ApplicationsDisease Models Animal030104 developmental biologyDrosophila melanogasterlcsh:Biology (General)lcsh:QD1-999coppermetal homeostasisDrosophilaDrosophila melanogasterheavy metal toxicityGenètica
researchProduct

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
researchProduct

The Role of NF-κB Triggered Inflammation in Cerebral Ischemia

2021

Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytoki…

0301 basic medicineMini ReviewIschemiaNeurosciences. Biological psychiatry. NeuropsychiatryContext (language use)InflammationBrain damageCervell Ferides i lesionsNeuroprotectionNF-κBcerebral ischemia03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinebusiness.industryNeurodegenerationneurodegenerationNF-κBInflammasomemedicine.disease030104 developmental biologychemistryinflammationCellular Neuroscienceneuroprotectionmedicine.symptombusinessOxigen Efectes fisiològicsNeuroscience030217 neurology & neurosurgeryRC321-571medicine.drugFrontiers in Cellular Neuroscience
researchProduct

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
researchProduct

DeepWAS: Multivariate genotype-phenotype associations by directly integrating regulatory information using deep learning

2020

Genome-wide association studies (GWAS) identify genetic variants associated with traits or diseases. GWAS never directly link variants to regulatory mechanisms. Instead, the functional annotation of variants is typically inferred by post hoc analyses. A specific class of deep learning-based methods allows for the prediction of regulatory effects per variant on several cell type-specific chromatin features. We here describe “DeepWAS”, a new approach that integrates these regulatory effect predictions of single variants into a multivariate GWAS setting. Thereby, single variants associated with a trait or disease are directly coupled to their impact on a chromatin feature in a cell type. Up to…

0301 basic medicineMultivariate analysisGene ExpressionGenome-wide association studyBiochemistry0302 clinical medicineGenotypeMedicine and Health SciencesBiology (General)0303 health sciencesDNA methylationEcologyChromosome BiologyNeurodegenerative DiseasesGenomicsChromatinChromatinNucleic acidsNeurologyComputational Theory and MathematicsModeling and SimulationDNA methylationTraitEpigeneticsDNA modificationFunction and Dysfunction of the Nervous SystemChromatin modificationResearch ArticleMultiple SclerosisQH301-705.5Quantitative Trait LociImmunologySingle-nucleotide polymorphismComputational biologyBiologyQuantitative trait locusPolymorphism Single NucleotideAutoimmune DiseasesMolecular Genetics03 medical and health sciencesCellular and Molecular NeuroscienceDeep LearningGenome-Wide Association StudiesGeneticsHumansGeneMolecular BiologyGenetic Association StudiesEcology Evolution Behavior and Systematics030304 developmental biologyGenetic associationBiology and Life SciencesComputational BiologyHuman GeneticsCell BiologyDNAGenome AnalysisDemyelinating Disorders030104 developmental biologyGenetic LociMultivariate AnalysisClinical ImmunologyClinical Medicine030217 neurology & neurosurgeryGenome-Wide Association StudyPLOS Computational Biology
researchProduct