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Inhibition of amyloid‐induced toxicity by ergothioneine in a transgenic Caenorhabditis elegans model
Author(s) -
Cheah Irwin K.,
Ng LiTheng,
Ng LiFang,
Lam Vanessa Y.,
Gruber Jan,
Huang Cheryl Y.W.,
Goh FangQin,
Lim Keith H.C.,
Halliwell Barry
Publication year - 2019
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13497
Subject(s) - caenorhabditis elegans , neuroprotection , oxidative stress , ergothioneine , neurotoxicity , genetically modified mouse , transgene , amyloid (mycology) , presenilin , biology , microbiology and biotechnology , toxicity , biochemistry , chemistry , antioxidant , pharmacology , alzheimer's disease , disease , medicine , pathology , botany , organic chemistry , gene
The abnormal accumulation of β‐amyloid peptide (Aβ) is recognized as a central component in the pathogenesis of Alzheimer disease. While many aspects of Aβ‐mediated neurotoxicity remain elusive, Aβ 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 Aβ‐toxicity in transgenic Caenorhabditis elegans overexpressing a human Aβ peptide. The accumulation of Aβ in this model leads to paralysis and premature death. We show that ET dose‐dependently reduces Aβ‐oligomerization and extends the lifespan and healthspan of the nematodes.