In Mouse Model of Alzheimer’s Disease, Specific Nanoparticles Successfully Suppressed Neuronal Death

In Mouse Model of Alzheimer’s Disease, Specific Nanoparticles Successfully Suppressed Neuronal Death
Scientists from the Center for Nanoparticle Research at South Korea's Institute for Basic Science (IBS), in collaboration with researchers at Seoul National University, have developed mitochondria-targeting ceria nanoparticles, a potential therapeutic candidate for mitochondrial oxidative stress and seen as one of the possible pathogenic pathways involved in the onset of Alzheimer’s disease. The research paper, “Mitochondria-Targeting Ceria Nanoparticles as Antioxidants for Alzheimer’s Disease,” was published in ACS Nano. Mitochondria are the energy-producing structures of the cell, converting nutrients into the molecule ATP, which is then used as energy, in a series of molecular reactions called the mitochondrial respiratory chain. This metabolic process requires oxygen and leads to the formation of reactive oxygen species (ROS) as a natural byproduct of the normal metabolism of oxygen. But mitochondrial dysfunction can lead to the abnormal production of ROS, which can lead to the death of neuronal cells. Importantly, amyloid beta (Aβ) plaque accumulation, one of the hallmarks of Alzheimer’s disease, has been shown to induce mitochondrial dysfunction, contributing to the overproduction of ROS and therefore a possible cause of Alzheimer’s. Researchers synthesized a mitochondria-specific antioxidant ceria nanoparticle, which is known to eliminate abnormal ROS, and investigated its effect in suppressing AD pathogenesis in an in vivo Alzheimer’s mouse model. The particles were successfully delivered to the mitochondria through the use of mitochondria-targeting materials.  The mice were injected a
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