New Alzheimer Disease Study Results Reported from School of Public Health (Uptake of silica nanoparticles: Neurotoxicity and Alzheimer-like pathology in human SK-N-SH and mouse neuro2a neuroblastoma cells)
By a News Reporter-Staff News Editor at Clinical Oncology Week -- Researchers detail new data in Neurodegenerative Diseases. According to news reporting originating in Guangdong, People's Republic of China, by NewsRx journalists, research stated, "Growing concern has been raised over the potential adverse effects of engineered nanoparticles on human health due to their increasing use in commercial and medical applications. Silica nanoparticles (SiNPs) are one of the most widely used nanoparticles in industry and have been formulated for cellular and non-viral gene delivery in the central nerve system."
The news reporters obtained a quote from the research from the School of Public Health, "However, the potential neurotoxicity of SiNPs remains largely unclear. In this study, we investigated the cellular uptake of SiNPs in human SK-N-SH and mouse neuro2a (N2a) neuroblastoma cells treated with 10.0 mu g/ml of 15-nm SiNPs for 24h by transmission electron microscopy. We found that SiNPs were mainly localized in the cytoplasm of the treated cells. The treatment of SiNPs at various concentrations impaired the morphology of SK-N-SH and N2a cells, characterized by increased number of round cells, diminishing of dendrite-like processes and decreased cell density. SiNPs significantly decreased the cell viability, induced cellular apoptosis, and elevated the levels of intracellular reactive oxygen species (ROS) in a dose-dependent manner in both cell lines. Additionally, increased deposit of intracellular p-amyloid 1-42 (A beta(1-42)) and enhanced phosphorylation of tau at Ser262 and Ser396, two specific pathological hallmarks of Alzheimer's disease (AD), were observed in both cell lines with SiNPs treatment. Concomitantly, the expression of amyloid precursor protein (APP) was up-regulated, while amyloid-beta-degrading enzyme neprilysin was down-regulated in SiNP-treated cells. Finally, activity-dependent phosphorylation of glycogen syntheses kinase (GSK)-3 beta at Ser9 (inactive form) was significantly decreased in SiNP-treated SK-N-SH cells. Taken together, these data demonstrated that exposure to SiNPs induced neurotoxicity and pathological signs of AD. The pre-Alzheimer-like pathology induced by SiNPs might result from the dys-regulated expression of APP/neprilysin and activation of GSK-3 beta."
According to the news reporters, the research concluded: "This is the first study with direct evidence indicating that in addition to neurotoxicity induced by SiNPs, the application of SiNPs might increase the risk of developing AD."
For more information on this research see: Uptake of silica nanoparticles: Neurotoxicity and Alzheimer-like pathology in human SK-N-SH and mouse neuro2a neuroblastoma cells. Toxicology Letters, 2014;229(1):240-249. Toxicology Letters can be contacted at: Elsevier Ireland Ltd, Elsevier House, Brookvale Plaza, East Park Shannon, Co, Clare, 00000, Ireland. (Elsevier - www.elsevier.com; Toxicology Letters - www.elsevier.com/wps/product/cws_home/505519)
Our news correspondents report that additional information may be obtained by contacting X.F. Yang, Southern Med Univ, Sch Public Hlth & Trop Med, Dept. of Occupat Hlth & Occupat Med, Guangzhou 510515, Guangdong, People's Republic of China. Additional authors for this research include C.E. He, J. Li, H.B. Chen, Q. Ma, X.J. Sui, S.L. Tian, M. Ying, Q. Zhang, Y.G. Luo, Z.X. Zhuang and J.J. Liu (see also Neurodegenerative Diseases).
Keywords for this news article include: Guangdong, People's Republic of China, Asia, Alzheimer Disease, Amyloid, Biological Tumor Markers, Brain Diseases, Central Nervous System Diseases, Dementia, Emerging Technologies, Hematology, Nanoparticle, Nanotechnology, Neprilysin, Neuroblastoma, Neurodegenerative Diseases, Oncology, Pathology, Proteins, Tauopathies
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