Ergothioneine protects against neuronal injury induced by β-amyloid in mice

Food Chem Toxicol. 2012 Nov;50(11):3902-11. doi: 10.1016/j.fct.2012.08.021. Epub 2012 Aug 16.


β-Amyloid peptides (Aβ) are neurotoxic and contribute to the development of Alzheimer's disease (AD). Ergothioneine (EGT) has been shown to protect against loss of memory and learning abilities in mice. In this study, mice were orally fed EGT (0.5 or 2 mg/kg body weight) for 16 days before treatment (i.c.v) with a single dose of Aβ1-40 in the hippocampus. After resting for 12 days to restore the body weight, the mice were again fed EGT for additional 39 days. Active avoidance tests were conducted on days 37-39 (short-memory avoidance) and on days 37, 44 and 51 (long-memory avoidance). Water maze task was used to evaluate learning and memory abilities by acquisition test and retention test. In both long-memory avoidance and water maze tests, EGT significantly decreased the escape latency and increased the frequency of successful avoidance. Furthermore, EGT significantly prevented Aβ accumulation in the hippocampus and brain lipid peroxidation, restored acetylcholinesterase (AChE) activity, maintained glutathione/glutathione disulfide ratio and superoxide dismutase activity in brain tissues of Aβ1-40-teated mice. Thus, EGT can protect against Aβ-induced loss of memory and learning abilities in mice. Further studies are required to confirm the protective effects of EGT on the development or progression of AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholinesterase / metabolism
  • Administration, Oral
  • Alzheimer Disease / drug therapy
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Avoidance Learning / drug effects
  • Brain / drug effects*
  • Brain / metabolism
  • Ergothioneine / administration & dosage
  • Ergothioneine / pharmacology*
  • Glutathione / metabolism
  • Glutathione Disulfide / metabolism
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Lipid Peroxidation / drug effects
  • Maze Learning / drug effects
  • Memory Disorders / prevention & control
  • Mice
  • Mice, Inbred C57BL
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neuroprotective Agents / pharmacology
  • Peptide Fragments / metabolism
  • Peptide Fragments / toxicity*
  • Superoxide Dismutase / metabolism


  • Amyloid beta-Peptides
  • Neuroprotective Agents
  • Peptide Fragments
  • amyloid beta-protein (1-40)
  • Ergothioneine
  • Superoxide Dismutase
  • Acetylcholinesterase
  • Glutathione
  • Glutathione Disulfide