Microglial cells and inflammatory cytokines in causation of Alzheimers disease.docVIP

Microglial cells and inflammatory cytokines in causation of Alzheimers disease.doc

  1. 1、原创力文档(book118)网站文档一经付费(服务费),不意味着购买了该文档的版权,仅供个人/单位学习、研究之用,不得用于商业用途,未经授权,严禁复制、发行、汇编、翻译或者网络传播等,侵权必究。。
  2. 2、本站所有内容均由合作方或网友上传,本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺!文档内容仅供研究参考,付费前请自行鉴别。如您付费,意味着您自己接受本站规则且自行承担风险,本站不退款、不进行额外附加服务;查看《如何避免下载的几个坑》。如果您已付费下载过本站文档,您可以点击 这里二次下载
  3. 3、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等,请点击“版权申诉”(推荐),也可以打举报电话:400-050-0827(电话支持时间:9:00-18:30)。
  4. 4、该文档为VIP文档,如果想要下载,成为VIP会员后,下载免费。
  5. 5、成为VIP后,下载本文档将扣除1次下载权益。下载后,不支持退款、换文档。如有疑问请联系我们
  6. 6、成为VIP后,您将拥有八大权益,权益包括:VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
  7. 7、VIP文档为合作方或网友上传,每下载1次, 网站将根据用户上传文档的质量评分、类型等,对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档
查看更多
Microglial cells and inflammatory cytokines in causation of Alzheimers disease

 PAGE \* MERGEFORMAT 18 Microglial cells and inflammatory cytokines in causation of Alzheimer’s disease [Keywords:] microglia cells; inflammatory cytokines; Alzheimer’s disease; causal relationship between Alzheimer’s disease (Alzheimer’s disease, AD) is a progressive degenerative neurons in the brain diseases, including familial AD and sporadic AD. Major clinical manifestations of progressive memory loss and cognitive impairment. Brain pathology is manifested mainly neurofibrillary tangles (neurafibrillarytangle, NFT) and senile plaques (senile plaque, SP) co-occurrence. Neurons within the NFT is the excessive TAU tubulin phosphorylation and glycosylation forms produced in the cell aggregation, whereas in the extracellular accumulation of SP mainly contains 40 ~ 42 amino acids of β -amyloid protein (amyloid β -protein, Aβ ) component. These pathological changes mainly in the parietal lobe, temporal lobe, frontal joint zones, such as the cerebral cortex, hippocampus and the forebrain. The majority of AD patients with brain Aβ to accumulate in the senile plaques Department, Aβ by β -amyloid precursor protein (amyloid precurso protein, APP) through a series of enzymatic reaction of a soluble product of degradation of APP is released [1]. The process of Aβ release by three kinds of enzymes to control, namely, α , β and γ -secretase [2], β -secretase in the Aβ domain of the first N-terminal methionine and aspartic acid cleavage between the release of a longer soluble APP fragment (solubleAPP-β , SAPP-β ), while the C terminal fragment was still with the (c-terminalfragment, CTF) membrane-bound, followed by γ -secretase cleavage CTF-β produced, ranging from the length of Aβ (39 ~ 43) amino acids, pathological significance of which is that Aβ 40 and Aβ 42 [3], brain Aβ 40 levels much higher than AB42, but Aβ 42 than Aβ 40 aggregation is not only faster, but the latter triggered by agglutination, is the main component of senile plaques. AD patients was fou

文档评论(0)

jiupshaieuk12 + 关注
实名认证
文档贡献者

该用户很懒,什么也没介绍

版权声明书
用户编号:6212135231000003

1亿VIP精品文档

相关文档