Peripheral manifestation of brain inflammation: signaling mechanisms
Peripheral manifestation of brain inflammation: signaling mechanisms
批准号:
10195319
负责人:
Qizhi Gong
金额:
$43.18万
依托单位国家:
美国
项目类别:
财政年份:
2021
资助国家:
美国
项目状态:
已结题
起止时间:
2021-04-15 至 2024-03-31
关键词:
AcuteAlzheimer disease detectionAlzheimer&aposs DiseaseAlzheimer&aposs disease patientAnatomyAnimal Disease ModelsAxonBrainCell SurvivalCell physiologyCellsClinicalCommunicationCytokine SignalingDataDepositionDevelopmentDiagnosticDisease ProgressionEarly DiagnosisEncephalitisEnvironmentEventFingerprintFutureGenetic TranscriptionGoalsIn VitroInflammationInflammatoryInjectionsInvestigationKnowledgeModelingMolecularMolecular MotorsNeurodegenerative DisordersNeuronal DifferentiationNeuropathyOlfactory EpitheliumOlfactory NerveOlfactory dysfunctionOrganPathogenesisPathogenicityPathway interactionsPeripheralPhysiologicalPhysiologyPresynaptic TerminalsProcessSenile PlaquesSignal TransductionSiteSupporting CellSystemTechniquesTestingTissuesToxic effectTransportationWild Type Mousecytokinein vitro Modelin vivoinsightneuroinflammationneuropathologyneurotrophic factorolfactory bulbolfactory sensory neuronsresponseretrograde transportsensory systemtranscriptome sequencing
中文摘要
项目摘要
嗅感觉神经元(Olfactory sensory neurons,OSNs)位于嗅上皮(olfactory epithelium,OE)内,将轴突直接传入嗅球
(OB)在大脑里。这一解剖学特征在所有感觉系统中是独一无二的,它使大脑直接暴露在
环境已知阿尔茨海默病(AD)的早期阶段反映在嗅觉功能障碍中。OB
大脑中的蛋白质含量显示了AD的早期神经病理学。众所周知,AD进展是
然而,目前还没有可靠的手段来早期检测与脑中神经炎症事件相关的神经系统炎症。
检测这些事件。我们的初步数据表明,OE响应于细胞因子水平的增加,
OB中的致病事件,可能通过经由嗅觉神经的逆行信号传导。逆行信号,
营养因子沿着轴突从末端到细胞体是众所周知的。我们假设OE是一种敏感的
通过嗅觉的逆行炎症细胞因子信号传导检测脑炎症的位点
神经。为了验证这一假设,我们将系统地描述转录变化的响应,
淀粉样斑块诱导炎症。将研究信号机制,以了解
关键的细胞过程。这项研究的长期目标是了解分子
神经退行性疾病中炎症的外周器官和脑通讯机制。
英文摘要
PROJECT SUMMARY
Olfactory sensory neurons (OSNs), residing in olfactory epithelium (OE), send axon directly into olfactory bulb
(OB) in the brain. This anatomical feature, unique among all sensory systems, exposes the brain directly to the
environment. It is known that early stages of Alzheimer Disease (AD) are reflected in olfactory dysfunction. OB
in the brain shows very early neuropathology in AD. It is well-established knowledge that AD progression is
correlated with neuroinflammatory events in the brain, however, there is currently no reliable means for early
detection of these events. Our preliminary data indicate that OE responds to increased levels of cytokines and
pathogenic events in the OB, likely through retrograde signaling via the olfactory nerve. Retrograde signaling to
trophic factors along axons from terminal to cell body is well known. We hypothesize that OE is a sensitive
site to detect brain inflammation via retrograde inflammatory cytokine signaling through the olfactory
nerve. To test this hypothesis, we will systematically characterize transcriptional changes in responding
amyloid plaque induced inflammation. Signaling mechanisms will be investigated to gain understanding of
critical cellular processes involved. The long-term goal of this study is to gain understanding of the molecular
mechanisms of peripheral organ and brain communication of inflammation in neurodegenerative diseases.
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会议论文
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资助金额:$32.56万
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财政年份:2010
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Role of MeCP2 in Circuitry Development and Plasticity
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Regulation of Odorant Receptor Gene Expression in Olfactory Sensory Neurons
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资助金额:$19.13万
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财政年份:2009
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Regulation of Odorant Receptor Gene Expression in Olfactory Sensory Neurons
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资助金额:$9.56万
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Regulation of Odorant Receptor Gene Expression in Olfactory Sensory Neurons
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资助金额:$33.17万
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依托单位:
DEVELOPMENT OF OLFACTORY CONNECTIONS
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DEVELOPMENT OF OLFACTORY CONNECTIONS
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资助金额:$31.45万
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财政年份:2003
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依托单位:
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依托单位:
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批准号:6616858
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资助金额:$7.43万
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财政年份:2001
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依托单位:
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