Nanoparticles as potential clinical therapeutic agents in Alzheimer’s disease: focus on selenium nanoparticles
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Nazıroğlu, Mustafa
Neuroscience Research Center, Suleyman Demirel University, Isparta, Turkey
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Muhamad, Salina
NANO Elec-Tronic Centre, Faculty of Electrical Engineering, Universiti Teknologi MARA, Shah Alam, Selangor, Malaysia
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Pecze, László
Institute of Anatomy, Department of Medicine, University of Fribourg, Switzerland
Published in:
- Expert Review of Clinical Pharmacology. - 2017, vol. 10, no. 7, p. 773–782
English
In etiology of Alzheimer’s disease (AD), involvement of amyloid β (Aβ) plaque accumulation and oxidative stress in the brain have important roles. Several nanoparticles such as titanium dioxide, silica dioxide, silver and zinc oxide have been experimentally using for treatment of neurological disease. In the last decade, there has been a great interest on combination of antioxidant bioactive compounds such as selenium (Se) and flavonoids with the oxidant nanoparticles in AD. We evaluated the most current data available on the physiological effects of oxidant and antioxidant nanoparticles.Areas covered: Oxidative nanoparticles decreased the activities of reactive oxygen species (ROS) scavenging enzymes such as glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase in the brain of rats and mice. However, Se-rich nanoparticles in small size (5–15 nm) depleted Aβ formation through decreasing ROS production. Reports on low levels of Se in blood and tissue samples and the low activities of GSH-Px, catalase and SOD enzymes in AD patients and animal models support the proposed crucial role of oxidative stress in the pathogenesis of AD.In conclusion, present literature suggests that Se-rich nanoparticles appeared to be a potential therapeutic compound for the treatment of AD.
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Faculty
- Faculté des sciences et de médecine
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Department
- Département de Médecine
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Language
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Classification
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Biological sciences
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License
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License undefined
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Identifiers
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Persistent URL
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https://folia.unifr.ch/unifr/documents/305678
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