Antagonizing beta-amyloid peptide neurotoxicity of the anti-aging fungus Ganoderma lucidum

Brain Res. 2008 Jan 23:1190:215-24. doi: 10.1016/j.brainres.2007.10.103. Epub 2007 Nov 13.


Ganoderma lucidum (Leyss. ex Fr.) Karst. (Lingzhi) is a medicinal fungus used clinically in many Asian countries to promote health and longevity. Synaptic degeneration is another key mode of neurodegeneration in Alzheimer's disease (AD). Recent studies have shown the loss of synaptic density proteins in each individual neuron during the progression of AD. It was recently reported that beta-amyloid (Abeta) could cause synaptic dysfunction and contribute to AD pathology. In this study, we reported that aqueous extract of G. lucidum significantly attenuated Abeta-induced synaptotoxicity by preserving the synaptic density protein, synaptophysin. In addition, G. lucidum aqueous extract antagonized Abeta-triggered DEVD cleavage activities in a dose-dependent manner. Further studies elucidated that phosphorylation of c-Jun N-terminal kinase, c-Jun, and p38 MAP kinase was attenuated by G. lucidum in Abeta-stressed neurons. Taken together, the results prove a hypothesis that anti-aging G. lucidum can prevent harmful effects of the exterminating toxin Abeta in AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / metabolism
  • Alzheimer Disease / prevention & control*
  • Amyloid beta-Peptides / drug effects*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Drugs, Chinese Herbal / pharmacology*
  • Medicine, East Asian Traditional*
  • Neurites / drug effects
  • Neurites / metabolism
  • Neurites / pathology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Neurons / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Reishi / chemistry
  • Synapses / drug effects
  • Synapses / metabolism
  • Synaptophysin / drug effects*
  • Synaptophysin / metabolism


  • Amyloid beta-Peptides
  • Drugs, Chinese Herbal
  • Synaptophysin