Mitochondria-Targeting Ceria Nanoparticles as Antioxidants for Alzheimeŕs Disease

  • Kwon H
  • Cha M
  • Kim D
 et al. 
  • 52


    Mendeley users who have this article in their library.
  • 48


    Citations of this article.


Mitochondrial oxidative stress is a key pathologic factor in neurodegenerative diseases, including Alzheimer's disease. Abnormal generation of reactive oxygen species (ROS), resulting from mitochondrial dysfunction, can lead to neuronal cell death. Ceria (CeO2) nanoparticles are known to function as strong and recyclable ROS scavengers by shuttling between Ce(3+) and Ce(4+) oxidation states. Consequently, targeting ceria nanoparticles selectively to mitochondria might be a promising therapeutic approach for neurodegenerative diseases. Here, we report the design and synthesis of triphenylphosphonium-conjugated ceria nanoparticles that localize to mitochondria and suppress neuronal death in a 5XFAD transgenic Alzheimer's disease mouse model. The triphenylphosphonium-conjugated ceria nanoparticles mitigate reactive gliosis and morphological mitochondria damage observed in these mice. Altogether, our data indicate that the triphenylphosphonium-conjugated ceria nanoparticles are a potential therapeutic candidate for mitochondrial oxidative stress in Alzheimer's disease.

Author-supplied keywords

  • Alzheimeŕs disease
  • ceria nanoparticles
  • mitochondria
  • reactive oxygen species
  • therapeutic agents

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • Hyek Jin Kwon

  • Moon Yong Cha

  • Dokyoon Kim

  • Dong Kyu Kim

  • Min Soh

  • Kwangsoo Shin

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free