• D C Zamberlan, L P Arantes, M L Machado, R Golombieski, and F A A Soares.
• Centro de Ciências Naturais e Exatas, Departamento de Química, Programa de Pós-graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
• Neuroscience. 2014 Oct 10; 278: 40-50.

AbstractAlzheimer's disease (AD) is the most common and devastating neurodegenerative disease. The etiology of AD has yet to be fully understood, and common treatments remain largely non-efficacious. The amyloid hypothesis posits that extracellular amyloid-β (Aβ) deposits are the fundamental etiological factor of the disease. The present study tested the organoselenium compound diphenyl-diselenide (PhSe)2, which is characterized by its antioxidant and antiinflammatory properties and has shown efficacy in several neurodegenerative disease models. We employed a transgenic Caenorhabditis elegans AD model to analyze the effects of (PhSe)2 treatment on Aβ peptide-induced toxicity. Chronic exposure to (PhSe)2 attenuated oxidative stress induced by Aβ1-42, with concomitant recovery of associative learning memory in C. elegans. Additionally, (PhSe)2 decreased Aβ1-42 transgene expression, suppressed Aβ1-42 peptide, and downregulated hsp-16.2 by reducing the need for this chaperone under Aβ1-42-induced toxicity. These observations suggest that (PhSe)2 plays an important role in protecting against oxidative stress-induced toxicity, thus representing a promising pharmaceutical modality that attenuates Aβ1-42 expression. Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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