Fucoidan inhibits amyloid-β-induced toxicity in transgenic Caenorhabditis elegans by reducing the accumulation of amyloid-β and decreasing the production of reactive oxygen species.

Abstract

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. As the aging population is increasing, AD is becoming one of the leading causes of disability and death among the elderly. However, currently there is no cure for this disease. Fucoidan is a complex sulfated polysaccharide mainly found in brown seaweed. Recent studies have shown that fucoidan is neuroprotective and may have potential to be used for treating and/or preventing neurodegenerative diseases such as AD. In this study, we investigated the effects and possible mechanisms of fucoidan on Abeta induced toxicity in a transgenic Caenorhabditis elegans (C. elegans) AD model. The results showed that the supplementation of fucoidan alleviated the paralyzed phenotype induced by Abeta. The number of Abeta deposits in the AD animals was reduced by fucoidan treatment. Further analysis of the levels of Abeta showed that fucoidan significantly decreased the accumulation of Abeta in transgenic AD C. elegans. It was found that fucoidan treatment elevated the activity of proteosomes; therefore, fucoidan might decrease Abeta accumulation by promoting proteolysis. In addition, fucoidan treatment reduced the production of reactive oxygen species (ROS) stimulated by Abeta induction. These results suggested that fucoidan might exert its protective effects against Abeta-induced toxicity in transgenic AD C. elegans by reducing the accumulation of toxic Abeta and decreasing Abeta-induced production of ROS, thus ameliorating the progression of the AD phenotype.