Search results for "tic disorder"

showing 10 items of 284 documents

Evidence against linkage of schizophrenia to chromosome 5q11-q13 markers in systematically ascertained families.

1992

Ten pedigrees systematically ascertained in Germany were tested for linkage to chromosome 5q11-q13. In order to replicate the previous report by Sherrington et al (1988), families with a bipolar family member were omitted from the lod score calculations, all diagnoses were based upon Research Diagnostic Criteria, and four different models of the affection status were calculated, including the model for which Sherrington et al calculated the highest lod scores. None of the families investigated showed a positive lod score. Using multipoint linkage analyses, we were able to exclude the region for which a positive linkage has been reported.

Linkage (software)GeneticsGenetic Markerscongenital hereditary and neonatal diseases and abnormalitiesGenetic LinkageResearch Diagnostic CriteriaPedigree chartmedicine.diseaseFamily memberChromosome (genetic algorithm)Psychotic DisordersSchizophreniamedicineSchizophreniaChromosomes Human Pair 5HumansFamilyLymphocytesLod ScorePsychologyBiological PsychiatryLod scoresLod scoreBiological psychiatry
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Variant recurrence in neurodevelopmental disorders: the use of publicly available genomic data identifies clinically relevant pathogenic missense var…

2019

Next-generation sequencing has revealed the major impact of de novo variants (DNVs) in developmental disorders (DD) such as intellectual disability, autism, and epilepsy. However, a substantial fraction of these predicted pathogenic DNVs remains challenging to distinguish from background DNVs, notably the missense variants acting via nonhaploinsufficient mechanisms on specific amino acid residues. We hypothesized that the detection of the same missense variation in at least two unrelated individuals presenting with a similar phenotype could be a powerful approach to reveal novel pathogenic variants. We looked for variations independently present in both our database of >1200 solo exomes and…

Male0301 basic medicineCandidate geneDevelopmental DisabilitiesMutation Missense030105 genetics & heredityBiology03 medical and health sciencesNeurodevelopmental disorderIntellectual DisabilityDatabases GeneticIntellectual disabilitymedicineHumansMissense mutationExomeGenetic Predisposition to DiseaseGenetic TestingAutistic DisorderGeneGenetics (clinical)Exome sequencingGeneticsComputational BiologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAmedicine.diseasePhenotype030104 developmental biologyNeurodevelopmental DisordersAutismFemaleTranscription FactorsGenetics in Medicine
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Lipoprotein-associated phospholipase A₂ activity is increased in patients with definite familial hypercholesterolemia compared with other forms of hy…

2018

International audience; Background and Aim: Lipoprotein-associated phospholipase A2 (Lp-PLA2) plays a key role in atherosclerosis development. It is considered a marker of increased risk of cardiovascular disease (CVD) and plaque vulnerability. Familial hypercholesterolemia (FH) is a genetic disorder characterized by elevated plasma levels of low-density lipoprotein cholesterol and a higher prevalence of early CVD. Our aim was to evaluate the differences in Lp-PLA2 activity in a population of hypercholesterolemic patients with and without definite FH.Methods and Results: Hypercholesterolemic patients were consecutively recruited. Definite FH was defined according to Dutch Lipid Clinic Netwo…

Male0301 basic medicineEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Low density lipoproteinDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematologyGastroenterologychemistry.chemical_compound0302 clinical medicineVascular inflammationeducation.field_of_studyNutrition and Dieteticsmedicine.diagnostic_testGenetic disorderMiddle Aged[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismCardiovascular diseaseLipidsUp-Regulation3. Good healthPhenotypeLow-density lipoproteinApolipoprotein B-100Femalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyStatin treatmentHypercholesterolemiaFamilial hypercholesterolemiaPopulationPhysical examinationHyperlipoproteinemia Type II03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineHumansLipoprotein-associated phospholipase A2Plaque vulnerabilityeducationAgedApolipoprotein A-Ibusiness.industryCholesterol HDLCholesterol LDLStatin treatmentAtherosclerosisCardiovascular riskmedicine.diseaseCross-Sectional Studies030104 developmental biologychemistry1-Alkyl-2-acetylglycerophosphocholine EsteraseHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessBiomarkersLipoproteinNutrition, Metabolism and Cardiovascular Diseases
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First report of X-linked hypohidrotic ectodermal dysplasia with a hemizygous c.1142G > C in the EDA gene: variant of uncertain significance or new pa…

2021

AbstractBackgroundHypohidrotic Ectodermal Dysplasia (HED) is a genetic disorder which affects structures of ectodermal origin. X-linked hypohidrotic ectodermal dysplasia (XLHED) is the most common form of disease. XLHED is characterized by hypotrichosis, hypohydrosis and hypodontia. The cardinal features of classic HED become obvious during childhood.Identification of a hemizygous EDA pathogenic variant in an affected male confirms the diagnosis.Case presentationWe report on a male newborn with the main clinical characteristics of the X-linked HED including hypotrichosis, hypodontia and hypohidrosis. Gene panel sequencing identified a new hemizygous missense variant of uncertain significanc…

Male0301 basic medicineProbandMutation MissenseVariants of uncertain significance (VUS)Case ReportX-linked.030105 genetics & heredityPediatricsRJ1-57003 medical and health sciencesEDA geneHumansMedicineMissense mutationHypohidrotic ectodermal dysplasiaX chromosomeHemizygoteGeneticsX-linkedChromosomes Human XEctodermal Dysplasia 1 Anhidroticbusiness.industryInfant NewbornGenetic disorderGeneral MedicineEctodysplasinsmedicine.diseaseHypoidrotic ectodermal dysplasiaHypodontia030104 developmental biologyHypotrichosisEctodysplasin AbusinessItalian Journal of Pediatrics
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Genetic contribution to the relationship between personality and depressive symptoms among older women.

2009

BackgroundPrior studies suggest that certain types of personality are at higher risk for developing depressive disorders. This study examined the relationship between old age depressive symptoms and two middle-age personality dimensions, neuroticism and extraversion.MethodThe present study is part of the Finnish Twin Study on Aging, where altogether 409 female twins who had completed the Eysenck Personality Inventory at the age of 38–51 years were studied for depressive symptoms 28 years later using Center for the Epidemiologic Studies Depression Scale. Logistic regression analysis suitable for dependent data and univariate and Cholesky models for decomposing the genetic and environmental f…

Male050103 clinical psychologyCharacterNeurotic Disordersmedia_common.quotation_subjectStatistics as TopicModels PsychologicalLogistic regressionDevelopmental psychologyCohort StudiesExtraversion Psychological03 medical and health sciences0302 clinical medicineRisk FactorsTwins DizygoticPersonalityHumans0501 psychology and cognitive sciencesGenetic Predisposition to DiseaseApplied PsychologyDepressive symptomsFinlandmedia_commonDepressive DisorderExtraversion and introversion05 social sciencesAge FactorsGender IdentityTwins MonozygoticNeuroticismTwin studyEysenck Personality QuestionnaireMiddle age030227 psychiatryPsychiatry and Mental healthCross-Sectional StudiesFemalePsychologyClinical psychologyPsychological medicine
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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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Treated Incidence of Psychotic Disorders in the Multinational EU-GEI Study

2018

Importance: Psychotic disorders contribute significantly to the global disease burden, yet the latest international incidence study of psychotic disorders was conducted in the 1980s. Objectives: To estimate the incidence of psychotic disorders using comparable methods across 17 catchment areas in 6 countries and to examine the variance between catchment areas by putative environmental risk factors. Design, Setting, and Participants: An international multisite incidence study (the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions) was conducted from May 1, 2010, to April 1, 2015, among 2774 individuals from England (2 catchment areas), France (3 catch…

Male2.3 Psychological social and economic factorsSYMPTOMS[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologyenvironmental risk factorsCatchment Area HealthRisk FactorsSCHIZOPHRENIADEPRIVATIONComputingMilieux_MISCELLANEOUShealth care economics and organizationsMinority Groups44 Human SocietyOriginal InvestigationNetherlands2 AetiologyOUTCOMES[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behaviorpsychotic disorders; international multisite incidence study; EU-GEI Study; environmental risk factorsIncidenceAge Factors[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive SciencesMental HealthEnglandItalyPsychiatry and Mental Health4206 Public Healthpopulation characteristicsFemaleFrancegeographic locationsBrazilAdultCross-Cultural ComparisonURBANICITYeducationAGESex Factorsparasitic diseasesHumans1ST-EPISODE PSYCHOSISRATESNOTTINGHAMinternational multisite incidence studyMETAANALYSISPublishingEU-GEI Study[SCCO.NEUR]Cognitive science/NeurosciencePrevention42 Health SciencesPsychotic DisordersSpainGene-Environment Interaction
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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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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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Substance-use disorder in high-functioning autism: clinical and neurocognitive insights from two case reports.

2014

Background Low prevalence of substance-use disorder has been reported in adults with autism. However, on a superficial level, adults with high-functioning autism (HFA) display a ‘normal’ façade when they drink alcohol, which may explain why their alcohol dependency is not better diagnosed. Case presentation Here, we report two cases of HFA adults who use alcohol and psychostimulants to cope with their anxiety and improve their cognitive abilities and social skills. We analyze how neurocognitive traits associated with HFA may be potential triggers for substance-use disorder. Conclusion Better identification of autism and its cognitive impairments, which may be vulnerability traits for develo…

MaleCognitive disabilitiesSubstance-Related DisordersAutismCase ReportMiddle Agedbehavioral disciplines and activitiesAnxiety DisordersAlcoholismmental disordersAdaptation PsychologicalSubstance-use disordersHumansCentral Nervous System StimulantsAutistic DisorderCognition DisordersAlcohol DeterrentsBMC psychiatry
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