中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (11): 1727-1728.doi: 10.4103/1673-5374.170288

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

细胞内APP分拣途径能否成为神经保护策略的思路?

  

  • 收稿日期:2015-10-08 出版日期:2015-12-07 发布日期:2015-12-07

Intracellular sorting pathways of the amyloid precursor protein provide novel neuroprotective strategies

Guido Hermey*   

  1. Institute for Molecular and Cellular Cognition, Center for Molecular
    Neurobiology Hamburg, University Medical Center
    Hamburg-Eppendorf, Hamburg, Germany
  • Received:2015-10-08 Online:2015-12-07 Published:2015-12-07
  • Contact: Guido Hermey, Ph.D.,guido.hermey@zmnh.uni-hamburg.de.

摘要:

德国汉堡大学医学中心,汉堡分子神经生物学中心Guido Hermey教授将淀粉样前蛋白和SorCS1共表达,未观察到淀粉样前蛋白在逆向运输中有任何重要的变化。然而,SorCS1c在囊泡顺向转运时保持淀粉样前蛋白,在囊泡静止时,淀粉样前蛋白有少量的增加。作者认为,未来的研究需要阐明这些变化是否由神经元中淀粉样前蛋白亚细胞靶点改变完成的?更多的研究也会包含细致地分析在SorCS1c敲除情况下淀粉样前蛋白在神经元中的传输。因此,了解细胞内APP分拣途径及其决定因素将会成为对阿尔茨海默病神经保护策略发展的基础。

Abstract:

Alzheimer’s disease (AD) is the most common cause of senile dementia. It is characterized by the formation of plaques mainly composed of the amyloid-beta peptide (Aβ). Diverse lines of evidence support the notion that accumulation of Aβ is a primary cause of AD pathogenesis. The current analyses suggest a model in which SorCS1 is not regulating Golgi-endosomal trafficking of APP, but is regulating its sorting and anterograde transport. Small alterations in APP trafficking may have a modest impact on Aβ generation, but probably result as a long-term effect over a lifetime in dramatic Aβ? accumulation. Therefore, understanding the intracellular sorting pathways of APP and its determinants in more detail will underlie the development of novel neuroprotective strategies.