Polysaccharides from Ganoderma lucidum Promote Cognitive Function and Neural Progenitor Proliferation in Mouse Model of Alzheimer's Disease

Stem Cell Reports. 2017 Jan 10;8(1):84-94. doi: 10.1016/j.stemcr.2016.12.007.


Promoting neurogenesis is a promising strategy for the treatment of cognition impairment associated with Alzheimer's disease (AD). Ganoderma lucidum is a revered medicinal mushroom for health-promoting benefits in the Orient. Here, we found that oral administration of the polysaccharides and water extract from G. lucidum promoted neural progenitor cell (NPC) proliferation to enhance neurogenesis and alleviated cognitive deficits in transgenic AD mice. G. lucidum polysaccharides (GLP) also promoted self-renewal of NPC in cell culture. Further mechanistic study revealed that GLP potentiated activation of fibroblast growth factor receptor 1 (FGFR1) and downstream extracellular signal-regulated kinase (ERK) and AKT cascades. Consistently, inhibition of FGFR1 effectively blocked the GLP-promoted NPC proliferation and activation of the downstream cascades. Our findings suggest that GLP could serve as a regenerative therapeutic agent for the treatment of cognitive decline associated with neurodegenerative diseases.

Keywords: Alzheimer's disease; Ganoderma lucidum; adult neurogenesis; cognition; fibroblast growth factor receptor 1.

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / psychology*
  • Animals
  • Cell Proliferation / drug effects
  • Cell Self Renewal / drug effects
  • Cognition / drug effects*
  • Disease Models, Animal
  • Fungal Polysaccharides / pharmacology*
  • Mice
  • Mice, Transgenic
  • Neural Stem Cells / drug effects*
  • Neural Stem Cells / metabolism*
  • Neurogenesis / drug effects
  • Receptor, Fibroblast Growth Factor, Type 1 / genetics
  • Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • Reishi / chemistry*
  • Signal Transduction / drug effects


  • Fungal Polysaccharides
  • Receptor, Fibroblast Growth Factor, Type 1