Mechanistic basis of inflammation in Alzheimers Disease
Mechanistic basis of inflammation in Alzheimers Disease
批准号:
10259772
负责人:
Amal O Amer
金额:
$18.47万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2020
资助国家:
美国
项目状态:
已结题
起止时间:
2020-09-15 至 2022-04-30
关键词:
Alzheimer&aposs DiseaseAlzheimer&aposs disease brainAlzheimer&aposs disease patientAlzheimer&aposs disease riskAmyloidAmyloid beta-ProteinAntisense OligonucleotidesAreaBrainCASP1 geneCASP4 geneCaspaseCellsCerebrospinal FluidComplexConfusionCytoskeletonDeteriorationExhibitsGene ProteinsGenetic VariationGrantHomologous GeneHousekeeping GeneHumanImmuneImpaired cognitionIn VitroIndividualInfectionInflammasomeInflammationInflammatoryInflammatory ResponseInterleukin-1 betaLabelLipopolysaccharidesLobeMediatingMemoryMicrogliaMusNeuraxisNeurodegenerative DisordersPatientsPreventionProductionPromoter RegionsProtein PrecursorsReportingReverse Transcriptase Polymerase Chain ReactionRoleSamplingSynaptic plasticityTestingUnited States National Institutes of HealthWild Type Mousebiobankbisulfite sequencingbrain tissuecytokinegenome wide methylationhigh riskin vivoinsightlearning abilitymemberoverexpressionpreventreceptor functionresponserisk variant
中文摘要
点击翻译按钮获取中文摘要
英文摘要
Abstract
Alzheimer’s disease (AD) is a progressive inflammatory neurodegenerative disorder leading to debilitating
cognitive dysfunction, and is still without cure or effective prevention options. Several studies demonstrated
that low grade inflammation in the brain is associated with higher risk of AD. Patients with AD exhibit an
overproduction of the pro-inflammatory cytokine interleukin-1 beta (IL-1β) in the cerebrospinal fluid and brain
tissue. Importantly, exaggerated IL-1β levels robustly inhibit synaptic plasticity mechanisms critical for normal
memory function. In this application we will determine the function of members of the canonical and non-
canonical inflammasome in relation of AD.
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