Affiliations: [a] Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, Lowell, MA 01854, USA | [b] Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA | [c] Department of Health and Clinical Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA | [d] Institute for Nano Science and Engineering Technology, Department of Chemistry, University of Massachusetts Lowell, Lowell, MA 01854, USA
Correspondence:
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Corresponding author: Thomas B. Shea, Ph.D., Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA. Tel.: +1 978 934 2881; Fax: +1 978 934 3044; E-mail: thomas_shea@uml.edu.
Abstract: Oxidative stress is an early hallmark of affected neurons in Alzheimer's disease (AD). The antioxidant vitamin E provided limited neuroprotection in AD, which may have derived from its lipophilic nature and resultant inability to quench cytosolic reactive oxygen species (ROS), including those generated from antecedent membrane oxidative damage. We examined herein whether or not encapsulation into polyethylene glycol (PEG)-based nanospheres, which can enter the cytosol, improved the efficacy of vitamin E against amyloid-β(Aβ)-induced ROS. Unexcapsulated vitamin E prevented Aβ-induced ROS in cultured SH-SY-5Y human neuroblastoma cells only if present prior to, or applied simultaneously with, Aβ treatment. By contrast, encapsulated vitamin E was equally effective if administered 1 hr after Aβ exposure. These findings suggest suggests that nanosphere-mediated delivery methods may be a useful adjunct for antioxidant therapy in AD.
Keywords: Amyloid-beta, antioxidants, vitamin E, nanospheres, Alzheimer's disease
