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Mar232016

Nanoparticle antioxidants offer potential Alzheimer’s therapy

Mitochondria have been known as a cell’s power plants. The abnormal generation of reactive oxygen species (ROS) from dysfunctioning mitochondria can cause neuronal cell death. This pathologic process is a key factor to a number of neurodegenerative diseases, including Alzheimer’s disease (AD). Amyloid-β peptides, which are believed to cause AD, can interact with resident proteins inside mitochondria, inducing abnormal production of ROS. Thus, ROS scavengers, such as antioxidant molecules, targeting mitochondria would be useful for prevention and early state treatment of AD.

A research team lead by Taeghwan Hyeon designed and synthesized triphenylphosphonium-conjugated ceria (CeO2) nanoparticles (TPP-ceria NPs), which can selectively localize in mitochondria and behave as strong ROS scavengers. These nanoparticles function in a recyclable manner by shuttling between Ce(III) and Ce(IV) oxidation states. The study of an AD mouse model indicates that the nanoparticles effectively suppress neuronal cell death by protecting them from ROS. This research has paved the road for the development of novel strategy to prevent and treat AD and other neurodegenerative diseases. 

WZ

Reference:

ACS Nano 2016, 10, 2860−2870.

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