Search results for "ddc:"

showing 10 items of 3080 documents

Characterizing the Molecular Architecture of Cortical Regions Associated with High Educational Attainment in Older Individuals

2019

Neuroimaging investigations have revealed interindividual variations in anatomy, metabolism, activity, and connectivity of specific cortical association areas through which years of education (YoE), as a common proxy of cognitive reserve, may operate in the face of age- or pathology-associated brain changes. However, the associated molecular properties of YoE-related brain regions and the biological pathways involved remain poorly understood. In the present study we first identified brain areas that showed an association between cortical thickness and YoE among 122 cognitively healthy older human individuals (87 female). We subsequently characterized molecular properties of these regions by…

0301 basic medicineMaleMicroarraymetabolism [Prefrontal Cortex]Prefrontal CortexNeuroimagingBiologyGyrus CinguliBiological pathway03 medical and health sciences0302 clinical medicineNeuroimagingCognitive ReserveCortex (anatomy)immunology [Gyrus Cinguli]metabolism [Gyrus Cinguli]Gene expressionmedicineHumansddc:610diagnostic imaging [Gyrus Cinguli]Prefrontal cortexResearch ArticlesCognitive reserveAgedGeneral NeuroscienceGene Expression ProfilingMiddle AgedMental Status and Dementia Testsphysiology [Cognitive Reserve]030104 developmental biologymedicine.anatomical_structureimmunology [Prefrontal Cortex]diagnostic imaging [Prefrontal Cortex]Educational StatusFemaleNeuroscience030217 neurology & neurosurgeryIonotropic effectGenome-Wide Association Study
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Autosomal-Recessive Mutations in AP3B2, Adaptor-Related Protein Complex 3 Beta 2 Subunit, Cause an Early-Onset Epileptic Encephalopathy with Optic At…

2016

International audience; Early-onset epileptic encephalopathy (EOEE) represents a heterogeneous group of severe disorders characterized by seizures, interictal epileptiform activity with a disorganized electroencephalography background, developmental regression or retardation, and onset before 1 year of age. Among a cohort of 57 individuals with epileptic encephalopathy, we ascertained two unrelated affected individuals with EOEE associated with developmental impairment and autosomal-recessive variants in AP3B2 by means of whole-exome sequencing. The targeted sequencing of AP3B2 in 86 unrelated individuals with EOEE led to the identification of an additional family. We gathered five addition…

0301 basic medicineMaleMicrocephalyDevelopmental DisabilitiesPostnatal microcephalycopper-metabolismEpilepsy0302 clinical medicineexpansionhermansky-pudlak-syndromeddc:576.5Age of OnsetChilddisordersGenetics (clinical)seizuresGeneticsMEDNIK syndromeSyndrome3. Good healthPedigreeintellectual disabilityChild Preschoolmednik syndromeMicrocephalyFemaleDevelopmental regressionAdaptor Protein Complex 3Genes RecessiveBiologyAP3B103 medical and health sciencesAtrophyReport[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansAdaptor Protein Complex beta SubunitsmousediseaseEpilepsyap-4 deficiencyInfant NewbornInfantmedicine.diseaseOptic Atrophy030104 developmental biologyMutationHermansky–Pudlak syndrome030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Dopamine neurons drive fear extinction learning by signaling the omission of expected aversive outcomes

2018

Extinction of fear responses is critical for adaptive behavior and deficits in this form of safety learning are hallmark of anxiety disorders. However, the neuronal mechanisms that initiate extinction learning are largely unknown. Here we show, using single-unit electrophysiology and cell-type specific fiber photometry, that dopamine neurons in the ventral tegmental area (VTA) are activated by the omission of the aversive unconditioned stimulus (US) during fear extinction. This dopamine signal occurred specifically during the beginning of extinction when the US omission is unexpected, and correlated strongly with extinction learning. Furthermore, temporally-specific optogenetic inhibition o…

0301 basic medicineMaleMouseExtinction PsychologicalPhotometry0302 clinical medicineFear conditioningBiology (General)extinctionGeneral NeuroscienceQRElectroencephalographyGeneral MedicineFearmusculoskeletal systemhumanitiesVentral tegmental areamedicine.anatomical_structureMedicineAnxietymedicine.symptomdopaminePsychologygeographic locationsmedicine.drugResearch ArticleQH301-705.5ScienceOptogeneticsUnconditioned stimulussafety learningGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesextinction ; fear conditioning ; safety learning ; dopamineDopaminemedicineAvoidance LearningAnimalsLearningddc:610General Immunology and MicrobiologyDopaminergic NeuronsVentral Tegmental AreaExtinction (psychology)social sciencesfear conditioningMice Inbred C57BLOptogeneticsElectrophysiology030104 developmental biologyNeuroscience030217 neurology & neurosurgeryNeuroscience
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Oligodendrocytes Provide Antioxidant Defense Function for Neurons by Secreting Ferritin Heavy Chain.

2020

An evolutionarily conserved function of glia is to provide metabolic and structural support for neurons. To identify molecules generated by glia and with vital functions for neurons, we used Drosophila melanogaster as a screening tool, and subsequently translated the findings to mice. We found that a cargo receptor operating in the secretory pathway of glia was essential to maintain axonal integrity by regulating iron buffering. Ferritin heavy chain was identified as the critical secretory cargo, required for the protection against iron-mediated ferroptotic axonal damage. In mice, ferritin heavy chain is highly expressed by oligodendrocytes and secreted by employing an unconventional secret…

0301 basic medicineMalePhysiologyAntioxidantsArticlemetabolism [Oligodendroglia]03 medical and health sciencesMyelinMice0302 clinical medicineddc:570medicineAnimalsSecretionReceptorCytotoxicityMolecular BiologySecretory pathwayNeuronsbiologyChemistrymetabolism [Apoferritins]Cell Biologybiology.organism_classificationCell biologyFerritinMice Inbred C57BLOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemmetabolism [Neurons]Apoferritinsbiology.proteinmetabolism [Antioxidants]Drosophila melanogaster030217 neurology & neurosurgeryFunction (biology)Cell metabolism
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Vitellogenin-like A–associated shifts in social cue responsiveness regulate behavioral task specialization in an ant

2018

Division of labor and task specialization explain the success of human and insect societies. Social insect colonies are characterized by division of labor, with workers specializing in brood care early and foraging later in life. Theory posits that this task switching requires shifts in responsiveness to task-related cues, yet experimental evidence is weak. Here, we show that a Vitellogenin (Vg) ortholog identified in an RNAseq study on the ant T. longispinosus is involved in this process: using phylogenetic analyses of Vg and Vg-like genes, we firstly show that this candidate gene does not cluster with the intensively studied honey bee Vg but falls into a separate Vg-like A cluster. Second…

0301 basic medicineMaleTask switchingAgingFat BodySocial SciencesGene ExpressionGenes InsectBiochemistryFatsVitellogeninsSociologyGene Regulatory NetworksForagingBiology (General)reproductive and urinary physiologyPhylogenyAnimal BehaviorBehavior AnimalGeneral NeuroscienceEukaryotaBeesLipidsANTInsectsAnimal SocialityGene Knockdown TechniquesMultigene FamilySocial SystemsInsect ProteinsFemaleCuesGeneral Agricultural and Biological SciencesHoney BeesDivision of labourResearch ArticleArthropodaQH301-705.5ForagingBiologyModels BiologicalGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesSpecies Specificityddc:570Specialization (functional)GeneticsAnimalsSocial BehaviorBehaviorGeneral Immunology and MicrobiologyAntsfungiOrganismsBiology and Life SciencesHoney beeSocial cueInvertebratesHymenopteraBrood030104 developmental biologyEvolutionary biologyZoologyPLoS Biology
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Dopamine, Noradrenaline and Serotonin Receptor Densities in the Striatum of Hemiparkinsonian Rats following Botulinum Neurotoxin-A Injection.

2017

Abstract Parkinson’s disease (PD) is characterized by a degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) that causes a dopamine (DA) deficit in the caudate-putamen (CPu) accompanied by compensatory changes in other neurotransmitter systems. These changes result in severe motor and non-motor symptoms. To disclose the role of various receptor binding sites for DA, noradrenaline, and serotonin in the hemiparkinsonian (hemi-PD) rat model induced by unilateral 6-hydroxydopamine (6-OHDA) injection, the densities of D1, D2/D3, α1, α2, and 5HT2A receptors were longitudinally visualized and measured in the CPu of hemi-PD rats by quantitative in vitro receptor autorad…

0301 basic medicineMalemedicine.medical_specialtyApomorphine5-HT2A receptorNeurotoxinsSubstantia nigraMotor ActivityFunctional LateralityAntiparkinson Agents03 medical and health sciences0302 clinical medicineDopamine receptor D1Parkinsonian DisordersDopamine receptor D3DopamineInternal medicinemedicineAnimalsddc:610Longitudinal StudiesBotulinum Toxins Type ARats WistarReceptorOxidopamine5-HT receptorChemistryGeneral NeuroscienceDopaminergicCorpus StriatumReceptors Neurotransmitter030104 developmental biologyEndocrinologyDopamine Agonists030217 neurology & neurosurgerymedicine.drugNeuroscience
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A multicentre, phase IIa study of zolbetuximab as a single agent in patients with recurrent or refractory advanced adenocarcinoma of the stomach or l…

2019

Abstract Background Claudin 18.2 (CLDN18.2) is physiologically confined to gastric mucosa tight junctions; however, upon malignant transformation, perturbations in cell polarity lead to CLDN18.2 epitopes being exposed on the cancer cell surface. The first-in-class monoclonal antibody, zolbetuximab (formerly known as IMAB362), binds to CLDN18.2 and can induce immune-mediated lysis of CLDN18.2-positive cells. Patients and methods Patients with advanced gastric, gastro-oesophageal junction (GEJ) or oesophageal adenocarcinomas with moderate-to-strong CLDN18.2 expression in ≥50% of tumour cells received zolbetuximab intravenously every 2 weeks for five planned infusions. At least three patients …

0301 basic medicineMalemedicine.medical_specialtyCLDN18.2Drug-Related Side Effects and Adverse ReactionsEsophageal NeoplasmsNauseagastro-oesophageal junction adenocarcinomaMedizinAdenocarcinomaGastroenterology03 medical and health sciences0302 clinical medicineStomach NeoplasmsInternal medicineGastrointestinal TumorsmedicineHumansProgression-free survivalAgedbusiness.industryStomachgastric cancerCancerAntibodies MonoclonalHematologyOriginal ArticlesMiddle Agedmedicine.diseaseddc:IMAB362030104 developmental biologymedicine.anatomical_structureTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisCohortVomitingAdenocarcinomaFemaleEsophagogastric Junctionmedicine.symptomzolbetuximabNeoplasm Recurrence Localbusiness
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Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

2017

Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated me…

0301 basic medicineMalememoriaAginggenetics [Stress Disorders Post-Traumatic]Diseasegenetics [Neuronal Plasticity]BioinformaticsdemenciaStress Disorders Post-TraumaticMice0302 clinical medicineRisk FactorsNews & ViewsAge of OnsetMice KnockoutNeuronal PlasticitybiologyGeneral NeuroscienceMicrofilament ProteinsNuclear Proteinsgenetics [Nuclear Proteins]FearadultoMiddle AgedAlzheimer's diseasephysiology [Aging]Phenotype3. Good healthPhenotypemiedoFormin 2Forminsgenetics [Aging]estres postraumaticoepidemiology [Stress Disorders Post-Traumatic]AdultHDAC inhibidorpsychology [Dementia]alzheimerForminsNerve Tissue Proteinsepidemiology [Dementia]Affect (psychology)General Biochemistry Genetics and Molecular Biology03 medical and health sciencesHDAC inhibitorMemorygenetics [Dementia]ddc:570medicineDementiaAnimalsHumansenvejecimientoMolecular Biologyphysiology [Memory]General Immunology and MicrobiologyPost-traumatic stress disordermedicine.diseaseYoung age030104 developmental biologyformin 2 protein mouseCase-Control StudiesSynaptic plasticitybiology.proteinDementiagenetics [Microfilament Proteins]complications [Stress Disorders Post-Traumatic]030217 neurology & neurosurgeryHomeostasis
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Impairment of Everyday Spatial Navigation Abilities in Mild Cognitive Impairment Is Weakly Associated with Reduced Grey Matter Volume in the Medial P…

2020

Alzheimer’s Disease Neuroimaging Initiative.

0301 basic medicineMalephysiopathology [Cognitive Dysfunction]positron emission tomographypathology [Cognitive Dysfunction]diagnostic imaging [Cognitive Dysfunction]grid cellsAudiologySpatial memoryVolumetry0302 clinical medicinepathology [Gray Matter]Activities of Daily Livingmagnetic resonance imagingEntorhinal CortexGray MatterAged 80 and overGeneral NeuroscienceGgrid cellsCognitionGeneral MedicineHuman brainOrgan SizeMiddle AgedMagnetic Resonance ImagingPsychiatry and Mental healthClinical Psychologymedicine.anatomical_structureFemalediagnostic imaging [Entorhinal Cortex]Spatial NavigationPositron emission tomographymedicine.medical_specialtyphysiology [Spatial Navigation]spatial navigationGrey matter03 medical and health sciencesAtrophymild cognitive impairmentNeuroimagingFluorodeoxyglucose F18medicineHumansCognitive Dysfunctionddc:610Entorhinal cortexAgedvolumetrybusiness.industrydiagnostic imaging [Gray Matter]Mild cognitive impairmentpathology [Entorhinal Cortex]Entorhinal cortexmedicine.disease030104 developmental biologyPositron-Emission TomographyBrodmann area 34Geriatrics and Gerontology18F-fluorodeoxyglucoseAtrophyRadiopharmaceuticalsbusiness030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Mismatch or allostatic load? Timing of life adversity differentially shapes gray matter volume and anxious temperament

2015

Traditionally, adversity was defined as the accumulation of environmental events (allostatic load). Recently however, a mismatch between the early and the later (adult) environment (mismatch) has been hypothesized to be critical for disease development, a hypothesis that has not yet been tested explicitly in humans. We explored the impact of timing of life adversity (childhood and past year) on anxiety and depression levels (N = 833) and brain morphology (N = 129). Both remote (childhood) and proximal (recent) adversities were differentially mirrored in morphometric changes in areas critically involved in emotional processing (i.e. amygdala/hippocampus, dorsal anterior cingulate cortex, res…

0301 basic medicineMalestressful life eventschildhood maltreatmentEmotionsAnxietySocial EnvironmentDevelopmental psychology0302 clinical medicineGray MatterVBMChildadversitymedia_commonDepressionAdult Survivors of Child AbuseAllostasisBrainGeneral MedicineOrgan SizeMagnetic Resonance ImagingAllostatic loadmedicine.anatomical_structureAllostasisAnxietyFemalemedicine.symptomPsychologymismatchallostatic loadAdultCognitive Neurosciencemedia_common.quotation_subjectExperimental and Cognitive PsychologyAffect (psychology)AmygdalaLife Change Events03 medical and health sciencesYoung AdultmedicineHumansddc:610TemperamentAnterior cingulate cortexBrain morphometryOriginal ArticlesImage Enhancement030104 developmental biologyTemperament030217 neurology & neurosurgerySocial Cognitive and Affective Neuroscience
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