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

Alzheimer’s disease (AD) is a neurological disease caused by the accumulation of extracellular senile plaques consisting of β-amyloid peptide (Aβ) in the brain. A transgenic Caenorhabditis elegans which demonstrated paralysis due to the expression of human beta amyloid Aβ42 gene was used to study th...

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Bibliographic Details
Main Authors: Chee wah yuen, Mardani Abdul Halim, Vikneswaran murugaiyah, Nazalan Najimudin, Ghows Azzam
Format: Article
Language:en
Published: Researchgate 2020
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Online Access:https://eprints.ums.edu.my/id/eprint/44355/1/FULL%20TEXT.pdf
https://eprints.ums.edu.my/id/eprint/44355/
http://dx.doi.org/10.1101/2020.04.13.040105
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Summary:Alzheimer’s disease (AD) is a neurological disease caused by the accumulation of extracellular senile plaques consisting of β-amyloid peptide (Aβ) in the brain. A transgenic Caenorhabditis elegans which demonstrated paralysis due to the expression of human beta amyloid Aβ42 gene was used to study the anti-paralysis effect of mixed tocotrienols. The content of the mixed tocotrienols were 12.1% α-, 2.7% β-, 18.6% γ-, and 8.1% δ-tocotrienols. Mixed tocotrienols significantly delayed the Aβ-induced paralysis in the transgenic nematode and exhibited anti-oxidant properties towards Aβ-generated oxidative stress. The mixture also presented potent inhibitory activities against Aβ 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.