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Mitochondria-Targeting Ceria Nanoparticles as Antioxidants for Alzheimer’s Disease

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Center for Nanoparticle Research, Institute for Basic Science (IBS), Seoul 151-742, Republic of Korea
School of Chemical and Biological Engineering and Institute of Chemical Processes, Seoul National University, Seoul 151-742, Republic of Korea
§ Department of Biochemistry and Biomedical Sciences, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea
Cite this: ACS Nano 2016, 10, 2, 2860–2870
Publication Date (Web):February 4, 2016
https://doi.org/10.1021/acsnano.5b08045
Copyright © 2016 American Chemical Society

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    Abstract

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    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 Ce3+ and Ce4+ 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.

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    • Additional results of nanoparticle characterization, in vitro studies, and Figures S1–S17 (PDF)

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