Neurobiology of Aggression Comorbidity in Autism
自闭症攻击性合并症的神经生物学
基本信息
- 批准号:10201418
- 负责人:
- 金额:$ 43.25万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-09-12 至 2022-05-31
- 项目状态:已结题
- 来源:
- 关键词:15q3-DimensionalAffectAggressive behaviorAllelesAxonBehavior DisordersBehavioralBindingBrainCell NucleusCellsChromosomesCommunicationComplexCopy Number PolymorphismCyclic AMP-Dependent Protein KinasesCytoplasmDataDefectDevelopmentDopamine AntagonistsDopamine D2 ReceptorElectroconvulsive TherapyElectrophysiology (science)EpitopesFDA approvedFamilyFeedbackFoundationsGene DosageGenesGeneticGenetic ModelsGenetic TranscriptionGlutamatesHumanHypothalamic structureInjectionsIsodicentric ChromosomeKnock-outLaboratoriesLearningLifeLightMapsMedicalMessenger RNAMissionModelingMolecularMusMutationNeurobiologyNeuronsNuclear ExportNuclear ImportPeptidesPharmaceutical PreparationsPhosphorylation SiteProblem behaviorRefractoryResearch DesignRoleSiteSocial InteractionSynapsesSynaptic TransmissionTerritorialityTestingTransgenic MiceUBE3A geneWorkautism spectrum disordercell typecomorbiditydesigner receptors exclusively activated by designer drugsdisabilityinsightinterstitialmalemimeticsneural circuitneuronal cell bodynew therapeutic targetnovelnovel therapeutic interventionpostsynapticpreclinical studyreceptorreconstitutionrepetitive behaviortherapeutic targettherapy developmenttooltransmission processubiquitin-protein ligase
项目摘要
PROJECT SUMMARY
Aggression is a frequent comorbidity in autism spectrum disorders (ASD). The problem is one of the
major reasons families seek medical therapy. Understanding the molecular basis and deciphering the neural
circuits that contribute to the development of this aggression comorbidity could inform novel targeted
therapeutics. Increased copies of maternal chromosome 15q11-13 region [interstitial duplication with a
single extra copy and extranumerary isodicentric chromosome 15q (Idic15) with two extra copies] are
frequent and strongly penetrant (Idic15) causes of ASD. We have recently established that extra copies
of Ube3a alone (15q11-13 gene expressed exclusively from maternal allele in neurons) are sufficient to
reproduce ASD-like deficits in mice (Smith et al. 2011). Interestingly, mice with extra copies of Ube3a
also show increased aggression. Taken together, these observations indicate that aberrant expression of
Ube3a underlies multiple ASD-associated behavioral problems. In this project we will dissect Ube3a's
role in controlling the aggression-comorbidity of ASD: 1) Identify specific neuronal cell types where
increased Ube3a gene dosage increase aggression and identify underlying transcriptional and
electrophysiological changes; and 2) Identify synaptic connections that are disrupted by increased Ube3a
gene dosage to increase aggression within those neuronal cell types. The project promotes the agency's
mission to further a deeper understanding of the neuronal cells, circuits, and genes involved in ASD via
genetic models. The novel molecular insights and genetic tools will facilitate development of treatments
for these life-long behavioral disabilities.
项目总结
项目成果
期刊论文数量(0)
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{{ truncateString('CLIFFORD B SAPER', 18)}}的其他基金
VTA VGluT2 Sociability Circuit in Genetic Autism
遗传性自闭症中的 VTA VGluT2 社交回路
- 批准号:
10091988 - 财政年份:2018
- 资助金额:
$ 43.25万 - 项目类别:
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