中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (8): 1562-1563.doi: 10.4103/1673-5374.303021

• 观点:退行性病与再生 • 上一篇    下一篇

从神经元过饱和角度探讨淀粉样蛋白假说

  

  • 出版日期:2021-08-15 发布日期:2021-01-13

Amyloid hypothesis through the lens of Aβ supersaturation

Zhefeng Guo*   

  1. Department of Neurology, Brain Research Institute, Molecular Biology Institute, University of California, Los Angeles, CA, USA
  • Online:2021-08-15 Published:2021-01-13
  • Contact: Zhefeng Guo, PhD, zhefeng@ucla.edu.
  • Supported by:
    This work was supported by the National Institute of Health, USA (No. R01AG050687).

摘要: https://orcid.org/0000-0003-1992-7255 
(Zhefeng Guo)

Abstract: Deposition of aggregated amyloid-β (Aβ) protein in the form of amyloid plaques is a pathological hallmark of Alzheimer’s disease. According to the amyloid hypothesis, Aβ aggregation initiates a pathogenic cascade, eventually leading to dementia. Being the prevailing theory for Alzheimer’s disease, amyloid hypothesis has been used to guide basic research and therapeutic interventions. Supersaturation is a phenomenon that occurs when the concentration of a solute in the solution exceeds its thermodynamic solubility. In the brain, Aβ proteins are usually supersaturated. Aβ aggregation follows the principle of supersaturation (So et al., 2016). In this perspective, I discuss the biochemical implications of Aβ supersaturation in the framework of amyloid hypothesis and how this knowledge can be used to improve therapeutic development for Alzheimer’s disease.