Tocotrienol decreases β-amyloid mediated toxicity in Caenorhabditis elegans model of Alzheimer's disease

Abstract

Alzheimers disease (AD) is a neurological disease caused by the accumulation of extracellular senile plaques consisting of {beta}-amyloid peptide (A{beta}) in the brain. A transgenic Caenorhabditis elegans which demonstrated paralysis due to the expression of human beta amyloid A{beta}42 gene was used to study the anti-paralysis effect of mixed tocotrienols. The content of the mixed tocotrienols were 12.1% -, 2.7% {beta}-, 18.6% {gamma}-, and 8.1% {delta}-tocotrienols. Mixed tocotrienols significantly delayed the A{beta}-induced paralysis in the transgenic nematode and exhibited anti-oxidant properties towards A{beta}-generated oxidative stress. The mixture also presented potent inhibitory activities against A{beta} aggregation with an IC50 value of 600 ng/ml. It is concluded that mixed tocotrienols could potentially serve as a new therapeutic candidate for AD.