Inhibition of amyloid-induced toxicity by ergothioneine in a transgenic Caenorhabditis elegans model

FEBS Letters

article

Irwin K. Cheah¹  Li-Theng Ng²  Li-Fang Ng³  Vanessa Y. Lam¹  Jan Gruber¹  Cheryl Y.W. Huang¹  Fang-Qin Goh¹  Keith H.C. Lim⁴  Barry Halliwell¹ 

[1] Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore;Life Science Institute, Neurobiology Programme, Centre for Life Sciences, National University of Singapore;Yale-NUS College;Department of Radiation Oncology, National University Health System, National University Cancer Institute Singapore

关键词: Alzheimer disease;    amyloid oligomerization;    antioxidant;    ergothioneine;    oxidative stress;    b-amyloid;   

DOI  :  10.1002/1873-3468.13497

来源: John Wiley & Sons Ltd.

【 摘 要 】

The abnormal accumulation of b-amyloid peptide (Ab) is recognized as a central component in the pathogenesis of Alzheimer disease. While many aspects of Ab-mediated neurotoxicity remain elusive, Ab has been associated with numerous underlying pathologies, including oxidative and nitrosative stress, inflammation, metal ion imbalance, mitochondrial dysfunction, and even tau pathology. Ergothioneine (ET), a naturally occurring thiol/thione-derivative of histidine, has demonstrated antioxidant and neuroprotective properties against various oxidative and neurotoxic stressors. This study investigates ET’s potential to counteract Ab-toxicity in transgenic Caenorhabditis elegans overexpressing a human Ab peptide. The accumulation of Ab in this model leads to paralysis and premature death. We show that ET dose-dependently reduces Ab-oligomerization and extends the lifespan and healthspan of the nematodes.

【 授权许可】

Unknown