Dystrophic functions of aged astrocytes following traumatic brain injury
Dystrophic functions of aged astrocytes following traumatic brain injury
批准号:
9434350
负责人:
Josh Morganti
金额:
$22.95万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2018
资助国家:
美国
项目状态:
已结题
起止时间:
2018-09-30 至 2020-05-31
关键词:
AcuteAdultAffectAgeAgingAlzheimer&aposs DiseaseAnimalsAstrocytesBehavioralBiological Response ModifiersBrainBrain InjuriesCCL2 geneCell SeparationChemotactic FactorsChronicCognitiveDataDementiaDevelopmentDiseaseEnvironmentEnvironmental Risk FactorEpidemicExperimental DesignsFlow CytometryGene ExpressionGenesGlial Fibrillary Acidic ProteinGoalsHealthcareHealthcare SystemsImpaired cognitionIncidenceIndividualInflammationInflammatoryInflammatory ResponseInjectionsInjuryKnowledgeLeukocytesLightLinkMagnetismMeasuresMediatingMicrogliaModelingMolecularMolecular ProfilingMusMyelogenousNerve DegenerationNeurodegenerative DisordersNeuronsOutcomeOutcome MeasureParkinson DiseasePathologicPathologyPathway interactionsPeripheralPopulationProductionRadialRecovery of FunctionResearch DesignResolutionRiskRisk FactorsRodentRoleSeveritiesSignal TransductionStimulusSurvivorsSynapsesTherapeuticTherapeutic InterventionTimeTraumatic Brain InjuryTraumatic Brain Injury recoveryUnited StatesWaterage effectagedaging brainaging populationarmcognitive functioncontrolled cortical impactcytokinedemographicsimprovedinflammatory milieuinjuredknowledge basemacrophagemonocytenano-stringneurotoxicnovelpreventrecruitresponseresponse to injuryrestorationtargeted treatmenttherapeutic targettranscription factoryoung adult
中文摘要
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英文摘要
The broad and long-term goals of this proposal are to form a significant knowledge-base
surrounding the role aged astrocytes in the propogation of neurodegenerative sequelae after TBI.
TBI in the aged population represents a significant unmet healthcare challenge, as advanced
aging is the greatest risk factor for acquiring a TBI, and subsequently developing
neurodegenerative disease such as dementia, Alzheimer’s- and Parkinson’s disease.
Cumulatively, the research design takes advantage of specific inflammatory hallmarks and
functional modulators associated with dystrophic astrocytes, in an attempt to delineate their
respective contributions to neuronal pathology and cognitive dysfunction. Ultimately, we will
determine if harnessing astrocytes via novel AAV constructs in aged TBI models is associated
with improving neuronal and cognitive outcome measures.
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会议论文
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海外基金