国际标准期刊号: 2161-0460

阿尔茨海默病和帕金森病杂志

开放获取

我们集团组织了 3000 多个全球系列会议 每年在美国、欧洲和美国举办的活动亚洲得到 1000 多个科学协会的支持 并出版了 700+ 开放获取期刊包含超过50000名知名人士、知名科学家担任编委会成员。

开放获取期刊获得更多读者和引用
700 种期刊 15,000,000 名读者 每份期刊 获得 25,000 多名读者

索引于
  • 哥白尼索引
  • 谷歌学术
  • 夏尔巴·罗密欧
  • 打开 J 门
  • Genamics 期刊搜索
  • 学术钥匙
  • 期刊目录
  • 中国知网(CNKI)
  • 电子期刊图书馆
  • 参考搜索
  • 哈姆达大学
  • 亚利桑那州EBSCO
  • OCLC-世界猫
  • SWB 在线目录
  • 虚拟生物学图书馆 (vifabio)
  • 普布隆斯
  • 日内瓦医学教育与研究基金会
  • 欧洲酒吧
  • ICMJE
分享此页面

抽象的

Chemokine Interleukin-8 (IL-8) in Alzheimer's and Other Neurodegenerative Diseases

James G McLarnon

Interleukin -8 (IL-8), a member of the CXC chemokine family, is well-documented as an important chemotactic signaling factor for recruitment of neutrophils to sites of infection and damage. However in neurodegenerative disease such as Alzheimer’s disease (AD), it is the resident macrophage cells, microglia, which are primary responding cells to brain insult such as deposition of amyloid β peptide. IL-8 exhibits an autocrine interaction with microglia by inducing a recruitment of the cells to specific sites of inflammation and subsequent increased production of the chemokine from activated cells. This positive feedback process thus has the capacity to amplify and sustain inflammatory response and brain neuroinflammation. The net result is that a localized and enhanced inflammatory response is induced by accumulating activated microglia at sites of inflammation serving to exacerbate inflammatory reactivity in AD brain. Importantly, under certain conditions the chemotaxis and subsequent activation of microglia may be deleterious to bystander cells including neurons. This review summarizes work from selected studies concerning the involvement and contributions of IL-8 mobilization from activated microglia to brain neuroinflammation as documented in the neurodegenerative diseases Alzheimer’s disease (AD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD).