Alzheimer’s Disease

Low levels of nerve growth factor (NGF) are seen in AD with implications for the application of Hericium erinaceus in the management of this condition (see discussion on Dementia)1. In addition, synaptic degeneration, with loss of synaptic density proteins, has been shown to be a key mode of neurodegeneration in AD with beta-amyloid (Abeta) identified as a cause of synaptic dysfunction and contributor to AD pathology.

Ganoderma lucidum aqueous extract, which has traditionally been considered to have anti-ageing properties, has been shown to significantly inhibit Abeta-induced synaptotoxicity and also inhibit Abeta-triggered DEVD cleavage in a dose-dependent manner with potential clinical application in management of AD and Auricularia polytricha, another mushroom considered to have anti-ageing properties, has been shown to inhibit the enzyme associated with release of Abeta2-3.

H. erinaceus fruiting body and G. lucidum extract can be combined in the treatment of AD. 3g/day H. erinaceus fruiting body with 1-2g/day G. lucidum extract.

1. Effects of Hericium erinaceus on amyloid β(25-35) peptide-induced learning and memory deficits in mice. Mori K, Obara Y, Moriya T, Inatomi S, Nakahata N. Biomed Res. 2011;32(1):67–72.
2. Heat-stable components of wood ear mushroom, Auricularia polytricha (higher Basidiomycetes), inhibit in vitro activity of beta secretase (BACE1). Bennett L, Sheean P, Zabaras D, Head R. Int J Med Mushrooms. 2013;15(3):233–249.
3. Antagonizing β-amyloid peptide neurotoxicity of the anti-ageing fungus Ganoderma lucidum. Lai CS, Yu MS, Yuen WH, So KF, Zee SY, Chang RC. Brain Res. 2008;1190:215–224.