Search results for "Polymicrogyria"

showing 10 items of 10 documents

The oculoauriculofrontonasal syndrome: Further clinical characterization and additional evidence suggesting a nontraditional mode of inheritance

2018

IF 2.264; International audience; The oculoauriculofrontonasal syndrome (OAFNS) is a rare disorder characterized by the association of frontonasal dysplasia (widely spaced eyes, facial cleft, and nose abnormalities) and oculo-auriculo-vertebral spectrum (OAVS)-associated features, such as preauricular ear tags, ear dysplasia, mandibular asymmetry, epibulbar dermoids, eyelid coloboma, and costovertebral anomalies. The etiology is unknown so far. This work aimed to identify molecular bases for the OAFNS. Among a cohort of 130 patients with frontonasal dysplasia, accurate phenotyping identified 18 individuals with OAFNS. We describe their clinical spectrum, including the report of new features…

0301 basic medicineMaleInheritance Patterns030105 genetics & heredityfrontonasal dysplasiawhole exome sequencingCraniofacial Abnormalities0302 clinical medicinePolymicrogyriaEye AbnormalitiesEar External10. No inequalityChildGenetics (clinical)Exome sequencingwhole genome sequencingThyroid agenesisHypoplasiaDNA-Binding ProteinsPhenotypeChild PreschoolFemaleRespiratory System Abnormalitiesmedicine.medical_specialtyAdolescentQuantitative Trait LociOculoauriculofrontonasal syndrome03 medical and health sciencesExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseFrontonasal dysplasiaGenetic Association StudiesWhole genome sequencingHomeodomain Proteinsbusiness.industryFacial cleftSkullInfant NewbornFaciesInfant030206 dentistrymedicine.diseaseDermatologySpine[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDysplasiabusinessTomography Spiral ComputedTranscription Factors
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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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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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Clinical and neuroimaging findings in 33 patients with MCAP syndrome: A survey to evaluate relevant endpoints for future clinical trials

2021

Megalencephaly-CApillary malformation-Polymicrogyria (MCAP) syndrome results from somatic mosaic gain-of-function variants in PIK3CA. Main features are macrocephaly, somatic overgrowth, cutaneous vascular malformations, connective tissue dysplasia, neurodevelopmental delay, and brain anomalies. The objectives of this study were to describe the clinical and radiological features of MCAP, to suggest relevant clinical endpoints applicable in future trials of targeted drug therapy. Based on a French collaboration, we collected clinical features of 33 patients (21 females, 12 males, median age of 9.9 years) with MCAP carrying mosaic PIK3CA pathogenic variants. MRI images were reviewed for 21 pat…

AdultMale0301 basic medicinePediatricsmedicine.medical_specialtyCutis marmorataAdolescentClass I Phosphatidylinositol 3-KinasesNeuroimagingContext (language use)Skin Diseases Vascular030105 genetics & heredityCohort StudiesYoung Adult03 medical and health sciencesGeneticsPolymicrogyriamedicineHumansPROSAbnormalities MultipleTelangiectasisMegalencephalyChildMCAP syndromeGenetics (clinical)Chiari malformationClinical Trials as Topicbusiness.industryMacrocephalyPIK3CAmedicine.diseaseMagnetic Resonance ImagingMegalencephaly3. Good healthClinical trial030104 developmental biologyChild PreschoolPostnatal macrocephalyFemalemedicine.symptombusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyForecastingVentriculomegalyClinical Genetics
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Both rare and de novo copy number variants are prevalent in agenesis of the corpus callosum but not in cerebellar hypoplasia or polymicrogyria.

2013

Agenesis of the corpus callosum (ACC), cerebellar hypoplasia (CBLH), and polymicrogyria (PMG) are severe congenital brain malformations with largely undiscovered causes. We conducted a large-scale chromosomal copy number variation (CNV) discovery effort in 255 ACC, 220 CBLH, and 147 PMG patients, and 2,349 controls. Compared to controls, significantly more ACC, but unexpectedly not CBLH or PMG patients, had rare genic CNVs over one megabase (p = 1.48×10−3; odds ratio [OR] = 3.19; 95% confidence interval [CI] = 1.89–5.39). Rare genic CNVs were those that impacted at least one gene in less than 1% of the combined population of patients and controls. Compared to controls, significantly more AC…

AdultMaleCancer ResearchMicrocephalycongenital hereditary and neonatal diseases and abnormalitiesAdolescentDNA Copy Number Variationslcsh:QH426-470Developmental DisabilitiesPopulationGenome-wide association studyBiologyNervous System MalformationsCorpus callosumPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineCerebellummental disordersGeneticsPolymicrogyriamedicineHumansCopy-number variationChildAgenesis of the corpus callosumeducationMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsExome sequencing030304 developmental biologyGenetics0303 health scienceseducation.field_of_studyGenome HumanInfant NewbornInfantMiddle Agedmedicine.disease3. Good healthMalformations of Cortical Developmentlcsh:GeneticsChild PreschoolFemaleAgenesis of Corpus Callosum030217 neurology & neurosurgeryResearch ArticleGenome-Wide Association StudyPLoS Genetics
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Pathogenic DDX3X mutations impair RNA metabolism and neurogenesis during fetal cortical development

2018

AbstractDe 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=78), demonstrating a striking correlation between recurrent dominant missense mutations, polymicrogyria, and the most severe clinical outcomes.…

GeneticsPathogenesisGermline mutationNeurogenesisPolymicrogyriamedicineMissense mutationTranslation (biology)BiologyDDX3Xmedicine.diseaseRNA Helicase A
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Megalencephaly Syndromes and Activating Mutations in the PI3K-AKT Pathway: MPPH and MCAP

2013

The megalencephaly‐polymicrogyria‐polydactyly‐hydrocephalus (MPPH) and megalencephaly‐capillary malformation (MCAP) syndromes are highly recognizable and partly overlapping disorders of brain overgrowth (megalencephaly). Both syndromes are characterized by congenital or early postnatal megalencephaly, with a high risk for progressive ventriculomegaly leading to hydrocephalus and cerebellar tonsillar ectopia leading to Chiari malformation, and cortical brain abnormalities, specifically polymicrogyria. MCAP is further characterized by distinct cutaneous capillary malformations, finger or toe syndactyly, postaxial polydactyly, variable connective tissue dysplasia and mild focal or segmental bo…

GeneticsPathologymedicine.medical_specialtyThymomaBiologymedicine.diseaseAKT3GermlineGermline mutationGeneticsPolymicrogyriamedicineMegalencephalyGenetics (clinical)PI3K/AKT/mTOR pathwayChiari malformationAmerican Journal of Medical Genetics Part C: Seminars in Medical Genetics
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Changes in the expression of cation-Cl- cotransporters, NKCC1 and KCC2, during cortical malformation induced by neonatal freeze-lesion.

2007

Focal cortical malformations comprise a heterogeneous group of disturbances in brain development, often associated with intractable epilepsy. A focal freeze-lesion of cerebral cortex in newborn rat produces a cortical malformation that resembles human polymicrogyria, clinical conditions that results from abnormal neuronal migration. The change in GABAergic functions that occurs during early brain development is induced by an alteration in Cl(-) homeostasis and plays important roles in neocortical development by modulating such events as laminar organization and synaptogenesis. We therefore investigated the relationship between pathogenesis of polymicrogyria and ontogeny of Cl(-) homeostasis…

MaleSodium-Potassium-Chloride SymportersSynaptogenesisDown-RegulationBiologyNervous System MalformationsLaminar organizationChloridesCell MovementChloride ChannelsCortex (anatomy)Parietal LobeGlial Fibrillary Acidic ProteinmedicinePolymicrogyriaAnimalsSolute Carrier Family 12 Member 2RNA MessengerRats Wistargamma-Aminobutyric AcidCerebral CortexSymportersGeneral NeuroscienceColocalizationCell DifferentiationGeneral Medicinemedicine.diseaseDenervationImmunohistochemistryMicrogyrusRatsUp-RegulationCold Temperaturemedicine.anatomical_structureNeuronal migration disorderBromodeoxyuridineCerebral cortexPhosphopyruvate HydrataseNeuroscienceBiomarkersNeuroscience research
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Gyrification from constrained cortical expansion

2014

The exterior of the mammalian brain - the cerebral cortex - has a conserved layered structure whose thickness varies little across species. However, selection pressures over evolutionary time scales have led to cortices that have a large surface area to volume ratio in some organisms, with the result that the brain is strongly convoluted into sulci and gyri. Here we show that the gyrification can arise as a nonlinear consequence of a simple mechanical instability driven by tangential expansion of the gray matter constrained by the white matter. A physical mimic of the process using a layered swelling gel captures the essence of the mechanism, and numerical simulations of the brain treated a…

Models AnatomicCompressive StrengthModels NeurologicalLissencephalyFOS: Physical sciencesGeometryPattern Formation and Solitons (nlin.PS)Condensed Matter - Soft Condensed MatterNerve Fibers MyelinatedWhite matterNeural PathwaysPolymicrogyriamedicineHumansDimethylpolysiloxanesPhysics - Biological PhysicsTissues and Organs (q-bio.TO)GyrificationCell ProliferationPhysicsCerebral CortexNeuronsMultidisciplinaryta114PachygyriaQuantitative Biology - Tissues and OrgansAnatomymedicine.diseaseNonlinear Sciences - Pattern Formation and SolitonsElasticitymedicine.anatomical_structureCerebral cortexBiological Physics (physics.bio-ph)FOS: Biological sciencesBrain sizePhysical SciencesSoft Condensed Matter (cond-mat.soft)Stress MechanicalBrain morphogenesisGels
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Branching enzyme deficiency/glycogenosis storage disease type IV presenting as a severe congenital hypotonia: muscle biopsy and autopsy findings, bio…

2010

The fatal infantile neuromuscular presentation of branching enzyme deficiency (glycogen storage disease type IV) due to mutations in the gene encoding the glycogen branching enzyme, is a rare but probably underdiagnosed cause of congenital hypotonia. We report an infant girl with severe generalized hypotonia, born at 33 weeks gestation who required ventilatory assistance since birth. She had bilateral ptosis, mild knee and foot contractures and echocardiographic evidence of cardiomyopathy. A muscle biopsy at 1 month of age showed typical polyglucosan storage. The autopsy at 3.5 months of age showed frontal cortex polymicrogyria and polyglucosan bodies in neurons of basal ganglia, thalamus, …

Pathologymedicine.medical_specialtyMuscle HypotoniaCardiomyopathyAutopsyGlycogen Storage Disease Type IVFatal Outcome14-alpha-Glucan Branching EnzymemedicineGlycogen branching enzymePolymicrogyriaHumansGlycogen storage disease type IVMuscle SkeletalGenetics (clinical)Muscle biopsymedicine.diagnostic_testbiologyInfant NewbornBrainInfantmedicine.diseaseNeurologyPediatrics Perinatology and Child Healthbiology.proteinMuscle HypotoniaFemaleNeurology (clinical)Differential diagnosisInfant PrematureNeuromuscular disorders : NMD
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