Abstract
In engineering and materials science, nanotechnology has made significant advances in the reduction of free radical damage. Despite such advances, there has been little application to biomedical problems. Cross-disciplinary interactions and the application of this technology to biological systems has led to the elucidation of novel nanoparticle antioxidants. Oxidative stress and free radical production are associated with neurodegenerative conditions, including aging, trauma, Alzheimers and Parkinsons diseases, etc. The antioxidant properties of cerium oxide nanoparticles show promise in the treatment of such diseases. Recent reports suggest that CeO2 and other nanoparticles are potent, and probably regenerative, free radical scavengers in vitro and in vivo. In this work, the effects of CeO2 nanoparticles on an in vitro human AD model are investigated. The validation of new therapeutic agents implies the understanding of their mechanisms of action, therefore the following parameters were investigated under nanoparticles treatment: cell viability, cell death, neurite atrophy, neuronal marker localization and the expression of factors, i.e. PPARβ, BDNF, TrkB, involved in the signal transduction pathways of neuronal survival. The data obtained, demonstrate that CeO2 nanoparticles do not act as mere anti-oxidant agents, but they seems to affect, directly or indirectly, signal transduction pathways involved in neuronal death and neuroprotection, raising the possibility of their use as therapeutic tools for neurodegenerative diseases.
Keywords: Cell viability, signal transduction mediators, antioxidant, oxidative stress, neurodegeneration
Current Nanoscience
Title: Cerium Oxide Nanoparticles Trigger Neuronal Survival in a Human Alzheimer Disease Model By Modulating BDNF Pathway
Volume: 5 Issue: 2
Author(s): Barbara D'Angelo, Sandro Santucci, Elisabetta Benedetti, Silvia Di Loreto, R. A. Phani, Stefano Falone, Fernanda Amicarelli, Maria Paola Ceru and Annamaria Cimini
Affiliation:
Keywords: Cell viability, signal transduction mediators, antioxidant, oxidative stress, neurodegeneration
Abstract: In engineering and materials science, nanotechnology has made significant advances in the reduction of free radical damage. Despite such advances, there has been little application to biomedical problems. Cross-disciplinary interactions and the application of this technology to biological systems has led to the elucidation of novel nanoparticle antioxidants. Oxidative stress and free radical production are associated with neurodegenerative conditions, including aging, trauma, Alzheimers and Parkinsons diseases, etc. The antioxidant properties of cerium oxide nanoparticles show promise in the treatment of such diseases. Recent reports suggest that CeO2 and other nanoparticles are potent, and probably regenerative, free radical scavengers in vitro and in vivo. In this work, the effects of CeO2 nanoparticles on an in vitro human AD model are investigated. The validation of new therapeutic agents implies the understanding of their mechanisms of action, therefore the following parameters were investigated under nanoparticles treatment: cell viability, cell death, neurite atrophy, neuronal marker localization and the expression of factors, i.e. PPARβ, BDNF, TrkB, involved in the signal transduction pathways of neuronal survival. The data obtained, demonstrate that CeO2 nanoparticles do not act as mere anti-oxidant agents, but they seems to affect, directly or indirectly, signal transduction pathways involved in neuronal death and neuroprotection, raising the possibility of their use as therapeutic tools for neurodegenerative diseases.
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Cite this article as:
D'Angelo Barbara, Santucci Sandro, Benedetti Elisabetta, Di Loreto Silvia, Phani A. R., Falone Stefano, Amicarelli Fernanda, Ceru Paola Maria and Cimini Annamaria, Cerium Oxide Nanoparticles Trigger Neuronal Survival in a Human Alzheimer Disease Model By Modulating BDNF Pathway, Current Nanoscience 2009; 5 (2) . https://dx.doi.org/10.2174/157341309788185523
DOI https://dx.doi.org/10.2174/157341309788185523 |
Print ISSN 1573-4137 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6786 |
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