Search results for "Autism."

showing 10 items of 454 documents

Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder

2017

AbstractGenetic risk factors for autism spectrum disorder (ASD) have yet to be fully elucidated. Postzygotic mosaic mutations (PMMs) have been implicated in several neurodevelopmental disorders and overgrowth syndromes. We systematically evaluated PMMs by leveraging whole-exome sequencing data on a large family-based ASD cohort, the Simons Simplex Collection. We found evidence that 11% of published single nucleotide variant (SNV)de novomutations are potentially PMMs. We then developed a robust SNV PMM calling approach that leverages complementary callers, logistic regression modeling, and additional heuristics. Using this approach, we recalled SNVs and found that 22% ofde novomutations like…

Male0301 basic medicineProbandZygoteautism spectrum disorderSYNGAP1Biologypostzygoticmedicine.disease_causeArticleGermlineCohort Studies03 medical and health sciencessplicing0302 clinical medicineNeurodevelopmental disorderGermline mutationDatabases GeneticGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationneurodevelopmentsomaticGenetic VariationExonsmedicine.disease030104 developmental biologymosaicism[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderCHD2AutismFemalemutation030217 neurology & neurosurgeryexome
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CNTN6 mutations are risk factors for abnormal auditory sensory perception in autism spectrum disorders

2017

International audience; Contactin genes CNTN5 and CNTN6 code for neuronal cell adhesion molecules that promote neurite outgrowth in sensory-motor neuronal pathways. Mutations of CNTN5 and CNTN6 have previously been reported in individuals with autism spectrum disorders (ASDs), but very little is known on their prevalence and clinical impact. In this study, we identified CNTN5 and CNTN6 deleterious variants in individuals with ASD. Among the carriers, a girl with ASD and attention-deficit/hyperactivity disorder was carrying five copies of CNTN5. For CNTN6, both deletions (6/1534 ASD vs 1/8936 controls; P=0.00006) and private coding sequence variants (18/501 ASD vs 535/33480 controls; P=0.000…

Male0301 basic medicinegenetic structuresAutism Spectrum Disorder[ SDV.MHEP.PSM ] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthmedicine.disease_causeChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGeneticsMutationPsychiatry and Mental healthSchizophrenia[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology[ SCCO.NEUR ] Cognitive science/NeuroscienceAuditory PerceptionMedical geneticsOriginal ArticleFemalePsychopharmacologymedicine.symptomPsychologyAdultmedicine.medical_specialtyAdolescentDNA Copy Number Variations[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsPolymorphism Single Nucleotidebehavioral disciplines and activities03 medical and health sciencesCellular and Molecular NeuroscienceContactinsmental disordersmedicineHumansDementiaGenetic Predisposition to DiseaseMolecular Biology[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceHyperacusis[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[ SDV.SP.PHARMA ] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologymedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAttention Deficit Disorder with Hyperactivity[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthMutationBehavioral medicine[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyAutismNeuroscienceMolecular Psychiatry
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A paradigmatic autistic phenotype associated with loss of PCDH11Y and NLGN4Y genes

2021

Abstract Background Most studies relative to Y chromosome abnormalities are focused on the sexual developmental disorders. Recently, a few studies suggest that some genes located on Y chromosome may be related to different neurodevelopment disorders. Case presentation We report a child with sexual developmental disorder associated with a peculiar phenotype characterized by severe language impairment and autistic behaviour associated with a mosaicism [45,X(11)/46,XY(89)] and a partial deletion of the short and long arm of Y chromosome (del Yp11.31q11.23) that also involves the loss of both PCDH11Y and NLGN4Y genes. To our knowledge no study has ever reported the occurrence of the lack of bot…

Male0301 basic medicinelcsh:Internal medicineMixed gonadal dysgenesilcsh:QH426-470Autism Spectrum DisorderCell Adhesion Molecules NeuronalNeuroliginProtocadherinCase ReportNeuroliginDevelopmental global delayBiologyY chromosome03 medical and health sciences0302 clinical medicineProtocadherinSettore M-PSI/08 - Psicologia ClinicaGeneticsmedicineHumanslcsh:RC31-1245ChildGenetics (clinical)GeneticsMosaicismMixed gonadal dysgenesismedicine.diseasePhenotypeSettore MED/39 - Neuropsichiatria InfantileHuman geneticsDevelopmental disorderlcsh:GeneticsPhenotype030104 developmental biologymedicine.anatomical_structureCerebral cortexAutism spectrum disorder030217 neurology & neurosurgeryBMC Medical Genomics
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A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
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The impact of sensory processing on executive and cognitive functions in children with autism spectrum disorder in the school context

2019

Abstract Background Theoretical approaches propose a hierarchical organization of sensory and higher-order cognitive processes, in which sensory processing influence some cognitive and executive functions. Aims The main objective of this study was to analyze whether sensory processing dysfunctions can predict the cognitive and executive dysfunctions evaluated in a group of children with level 2 autism spectrum disorder (ASD) in the school context. Methods and procedures Two groups of children participated: an ASD group (n = 40) and a group of children with typical development (the comparison group, n = 40). The children’s sensory processing was evaluated based on their teachers’ perceptions…

Male030506 rehabilitationSensory processingAutism Spectrum Disordermedicine.medical_treatmentmedia_common.quotation_subjectSensory systemContext (language use)behavioral disciplines and activitiesDevelopmental psychologyPerceptual Disorders03 medical and health sciencesExecutive FunctionCognitionPerceptionmental disordersDevelopmental and Educational PsychologymedicineHumans0501 psychology and cognitive sciencesChildmedia_commonSchools05 social sciencesCognitionmedicine.diseaseExecutive functionsClinical PsychologyPsicologiaAutism spectrum disorderCase-Control StudiesChild PreschoolFemaleVerbal memoryAutisme0305 other medical sciencePsychology050104 developmental & child psychology
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Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenot…

2021

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal lethality of germline knockout mice lacking the entire APP family has so far precluded the analysis of its physiological functions for the developing and adult brain. Here, we generated conditional APP/APLP1/APLP2 triple KO (cTKO) mice lacking the APP family in excitatory forebrain neurons from embryonic day 11.5 onwards. NexCre cTKO mice showed altered brain morphology with agenesis of the corpus callosum and disrupted hippocampal lamination. Further, NexCre cTKOs revealed reduced basal synaptic transmission and drastically reduced long-term potentiation that was associated with reduced dendritic length …

Male10017 Institute of AnatomyLong-Term PotentiationHippocampal formationSynaptic TransmissionAmyloid beta-Protein Precursor0302 clinical medicine2400 General Immunology and MicrobiologyAmyloid precursor proteinMolecular Biology of DiseaseAutism spectrum disorderMice KnockoutNeurons0303 health sciencesbiologyBehavior AnimalGeneral NeuroscienceBrain2800 General NeuroscienceLong-term potentiationArticlesPhenotype10076 Center for Integrative Human PhysiologyKnockout mouseFemalelearning and memory610 Medicine & healthGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesProsencephalon1300 General Biochemistry Genetics and Molecular Biologymental disorders1312 Molecular BiologyAnimalsLearningAPLP1Autistic DisorderSocial BehaviorMolecular BiologyAPLP2CA1 Region Hippocampal030304 developmental biologysynaptic plasticityGeneral Immunology and MicrobiologyAmyloid precursor proteinSynaptic plasticityForebrainSynapsesbiology.proteinAlzheimer570 Life sciences; biologyNeuroscience030217 neurology & neurosurgeryNeuroscienceThe EMBO journal
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Recollection in adolescents with Autism Spectrum Disorder.

2013

Abstract Introduction Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder primarily affecting social interaction and communication. Recently, there has been interest in whether people with ASD also show memory deficits as a result of abnormal brain development. However, at least in adolescents with ASD, the recollection component of episodic memory has rarely been explored. This paper is an evaluation of recollection in three different experiments in adolescents with ASD, using both objective (source discrimination) and subjective methods (Remember–Know judgments). Methods Three experiments were designed to measure different aspects of contextual information: sensory/perceptual …

MaleAdolescentCognitive Neurosciencemedia_common.quotation_subjectSensationExperimental and Cognitive PsychologyContext (language use)Neuropsychological Testsbehavioral disciplines and activitiesDevelopmental psychologyJudgmentNeurodevelopmental disorderDiscrimination PsychologicalMental ProcessesMemorymental disordersmedicineHumansQuality (business)Episodic memorymedia_commonIntelligence TestsAnalysis of VarianceRecallRecognition Psychologymedicine.diseaseSocial relationNeuropsychology and Physiological PsychologyAutism spectrum disorderChild Development Disorders PervasiveSpace PerceptionMental RecallAutismFemalePerceptionPsychologyPhotic StimulationPsychomotor PerformanceCognitive psychologyCortex; a journal devoted to the study of the nervous system and behavior
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Incomplete Gestation has an Impact on Cognitive Abilities in Autism Spectrum Disorder

2019

Extreme prematurity is known as a risk factor for autism spectrum disorder (ASD). However, the association between prematurity and ASD, for children born moderately and late preterm (MLPT) and those born early term (ET), is less established. This retrospective study aimed to characterize the phenotypic characteristics (i.e. behavioral profile and cognitive abilities) of 254 children with ASD, between 3 and 15 years of age, born MLPT (19 children), ET (60 children) and full term (175 children). MLPT and ET births do not modify ASD symptomatology, but modify cognitive development. The results highlight that incomplete gestation, i.e., MLPT or ET, has a negative impact on both verbal and nonve…

MaleAdolescentCognitive abilitiebehavioral disciplines and activities03 medical and health sciencesNonverbal communicationCognition0302 clinical medicinePregnancyModerately and late pretermmental disordersDevelopmental and Educational PsychologymedicineCognitive developmentHumans0501 psychology and cognitive sciencesAutism spectrum disorderRisk factorChildFull Term05 social sciencesInfant NewbornRetrospective cohort studyCognitionmedicine.diseaseAutism spectrum disorderChild PreschoolPremature BirthAutismFemaleCognition DisordersPsychologyEarly termInfant Premature030217 neurology & neurosurgery050104 developmental & child psychologyClinical psychologyJournal of Autism and Developmental Disorders
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Prognostic factors and predictors of outcome in children with autism spectrum disorder: the role of the paediatrician.

2021

Abstract Background Autism spectrum disorder is a complex condition with wide variation in type and severity that involves persistent challenges in social interaction, speech and nonverbal communication, restricted/repetitive behaviours and adaptive behaviours. In recent years, research has deepened the study of the predictive factors of optimal outcome, intended as indicators of positive trajectory in children with a previous diagnosis of autism who, after a therapeutic path, show a significant reduction in the “core” symptoms of autism and a positive evolution in social, adaptive, affective, and relational skills. Methods The study included 40 children aged 21 to 66 months, enrolled betwe…

MaleAutism Spectrum DisorderEmotionsIntelligenceEmotional contagionbehavioral disciplines and activities03 medical and health sciencesNonverbal communication0302 clinical medicinePaediatricianmental disordersmedicineHumans0501 psychology and cognitive sciencesPediatriciansPhysician's RoleRetrospective StudiesOutcomeIntelligence quotientbusiness.industryPredictorsResearch05 social scienceslcsh:RJ1-570InfantCognitionRetrospective cohort studylcsh:Pediatricsmedicine.diseasePrognosisSocial relationAutism spectrum disorderChild PreschoolAutismFemaleEmotional variablesbusiness030217 neurology & neurosurgeryPredictor050104 developmental & child psychologyClinical psychologyItalian journal of pediatrics
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The K63 deubiquitinase CYLD modulates autism-like behaviors and hippocampal plasticity by regulating autophagy and mTOR signaling.

2021

Nondegradative ubiquitin chains attached to specific targets via Lysine 63 (K63) residues have emerged to play a fundamental role in synaptic function. The K63-specific deubiquitinase CYLD has been widely studied in immune cells and lately also in neurons. To better understand if CYLD plays a role in brain and synapse homeostasis, we analyzed the behavioral profile of CYLD-deficient mice. We found that the loss of CYLD results in major autism-like phenotypes including impaired social communication, increased repetitive behavior, and cognitive dysfunction. Furthermore, the absence of CYLD leads to a reduction in hippocampal network excitability, long-term potentiation, and pyramidal neuron s…

MaleAutism Spectrum DisorderNerve Tissue ProteinsHippocampal formationHippocampusDeubiquitinating enzymeSynapseMiceUbiquitinAutophagyAnimalsAutistic DisorderMechanistic target of rapamycinPI3K/AKT/mTOR pathwayNeuronsMultidisciplinarybiologyUbiquitinLysineTOR Serine-Threonine KinasesAutophagyMicrofilament ProteinsUbiquitinationLong-term potentiationBiological SciencesDeubiquitinating Enzyme CYLDMice Inbred C57BLSynapsesbiology.proteinFemaleNeuroscienceSignal TransductionProceedings of the National Academy of Sciences of the United States of America
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