Clusterin in Alzheimer’s disease: a player in the biological behavior of amyloid-beta

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• 作者：Xiang Li (1)
  Yifei Ma (1)
  Xu Wei (1)
  Yanpeng Li (1)
  Huijuan Wu (1)
  Jianhua Zhuang (1)
  Zhongxin Zhao (1)
  
• 关键词：clusterin ; Alzheimer’s disease ; amyloid ; beta peptides ; cytotoxicity ; cytoprotection
• 刊名：Neuroscience Bulletin
• 出版年：2014
• 出版时间：February 2014
• 年：2014
• 卷：30
• 期：1
• 页码：162-168
• 全文大小：305 KB
• 作者单位：Xiang Li (1)
  Yifei Ma (1)
  Xu Wei (1)
  Yanpeng Li (1)
  Huijuan Wu (1)
  Jianhua Zhuang (1)
  Zhongxin Zhao (1)
  
  1. Department of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China
  
• ISSN：1995-8218

文摘

Alzheimer’s disease (AD) remains a major killer, and although its pathogenesis varies, one dominant feature is an increase in the expression, formation, and sedimentation of senile plaques of amyloid-beta (Aβ) peptides in the brain. The chaperone protein clusterin has, since its first discovery at the end of the 20th century, been labeled as a cytoprotector. However, epigenetic studies showing that clusterin is associated with the severity and risk of AD, especially in the hippocampus, triggered studies to clarify its role in the pathogenesis of AD. It is true that clusterin can inhibit the aggregation of Aβ and therefore prevent further formation of senile plaques in the AD brain, yet it induces the formation of soluble forms of Aβ which are toxic to neurons. Another problematic finding is that clusterin is involved in a pathway through which Aβ has neurodegenerative effects intracellularly. Although the role of clusterin in the pathogenesis of AD is still not clear, this review specifically discusses the interactions between clusterin and Aβ, to open up the possibility of a potential therapeutic approach for treating AD.