IMPORTANCE OF PERIODONTITIS IN THE INNATE IMMUNE REGULATION OF ALZHEIMER'S DISEASE

牙周炎在阿尔茨海默病先天免疫调节中的重要性

基本信息

  • 批准号:
    10658447
  • 负责人:
  • 金额:
    $ 37.13万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2023
  • 资助国家:
    美国
  • 起止时间:
    2023-06-01 至 2028-02-29
  • 项目状态:
    未结题

项目摘要

Project Summary/Abstract Albeit periodontal disease is a local chronic infectious inflammatory process affecting tissues supporting teeth, it can also have systemic consequences. Along these lines are reports that Alzheimer’s disease (AD) is epidemiologically associated with periodontal disease. Yet, the mechanisms underlying this association are not delineated. Our preliminary studies provide new evidence that a keystone periodontal pathogen Porphyromonas gingivalis (Pg) could enter the brain and exacerbate amyloid-b (Ab) accumulation, neuroinflammation, microglia activation, synapse loss, and cognitive and behavioral impairments in AD mice upon oral gavage infection. Microglia are the primary innate immune cells in the brain, and microglial activation is an invariable feature of AD pathology. The complement system also represents a major part of innate immunity, and microglia have been identified as the dominant source of C1q, the initiation factor of the classical complement pathway, in the brain. The objective of this application is to understand the importance of periodontitis in regulating microglial in AD, and the role of complement component C1q in microglial activation and AD progression. Based on the literature and our preliminary results, we hypothesize that periodontal infection and inflammation not only increase the severity of AD, but also increase the risk of AD, via potentiating Ab-primed microglial activation and sensitizing microglia for a heightened inflammatory response to subsequent pathogenic stimuli. In addition, periodontitis-associated persistent C1q activation is critical for microglial priming and activation, and the increased neurodegeneration in AD. We will test our hypothesis by pursuing two specific aims. Aim 1 will determine how periodontitis regulates microglial activation in AD using three different models of periodontitis. Aim 2 will determine the role of complement component C1q in microglial activation and AD development following Pg infection. Our proposed studies will provide novel and significant insights into the association between periodontal infection and AD. Understanding how a prevalent chronic infection like periodontitis modulates complement and microglial activation will advance our understanding of the mysterious etiology of AD. The knowledge obtained from these studies will provide a basis for targeting microbial etiology and periodontal therapy to ameliorate the clinical manifestations of AD and lower AD prevalence.
项目总结/文摘

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Ping Zhang其他文献

毛细管电泳差分非接触电导检测器测定氨基酸
  • DOI:
  • 发表时间:
    2012
  • 期刊:
  • 影响因子:
    6.1
  • 作者:
    Yaolong Li;Zhenli Zhang;Ping Zhang;Qi Kang
  • 通讯作者:
    Qi Kang

Ping Zhang的其他文献

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{{ truncateString('Ping Zhang', 18)}}的其他基金

ROLE OF OSTEOCLAST PRECURSORS IN PERIODONTAL BONE LOSS
破骨细胞前体在牙周骨丢失中的作用
  • 批准号:
    9381236
  • 财政年份:
    2017
  • 资助金额:
    $ 37.13万
  • 项目类别:
ROLE OF OSTEOCLAST PRECURSORS IN PERIODONTAL BONE LOSS
破骨细胞前体在牙周骨丢失中的作用
  • 批准号:
    10201568
  • 财政年份:
    2017
  • 资助金额:
    $ 37.13万
  • 项目类别:
Molecular mechanisms of the innate regulation of osteoclastogenesis.
破骨细胞生成先天调节的分子机制。
  • 批准号:
    8488432
  • 财政年份:
    2012
  • 资助金额:
    $ 37.13万
  • 项目类别:
Molecular mechanisms of the innate regulation of osteoclastogenesis.
破骨细胞生成先天调节的分子机制。
  • 批准号:
    8383398
  • 财政年份:
    2012
  • 资助金额:
    $ 37.13万
  • 项目类别:
Load-Driven Bone Lengthening
负载驱动的骨延长
  • 批准号:
    7847554
  • 财政年份:
    2008
  • 资助金额:
    $ 37.13万
  • 项目类别:
Load-Driven Bone Lengthening
负载驱动的骨延长
  • 批准号:
    7513232
  • 财政年份:
    2008
  • 资助金额:
    $ 37.13万
  • 项目类别:
Load-Driven Bone Lengthening
负载驱动的骨延长
  • 批准号:
    7670257
  • 财政年份:
    2008
  • 资助金额:
    $ 37.13万
  • 项目类别:
Mechanistic Analyses of kinase signaling complexes
激酶信号复合物的机制分析
  • 批准号:
    10486948
  • 财政年份:
  • 资助金额:
    $ 37.13万
  • 项目类别:
Mechanistic Analyses of kinase signaling complexes
激酶信号复合物的机制分析
  • 批准号:
    10926302
  • 财政年份:
  • 资助金额:
    $ 37.13万
  • 项目类别:
Structual and function of kinase signaling complexes
激酶信号复合物的结构和功能
  • 批准号:
    10262432
  • 财政年份:
  • 资助金额:
    $ 37.13万
  • 项目类别:

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