Mushrooms are considered not only as food but also for source of physiologically beneficial medicines. The culinarymedicinal mushrooms may important role in the prevention of age-associated neurological dysfunctions, including Alzheimer’s and Parkinson’s diseases. Hericium erinaceus (H. erinaceus), is edible mushrooms, is a parasitic fungus that grows hanging off of logs and trees and well established candidate for brain and nerve health. H. erinaceus contains high amounts of antioxidants, beta-glucan, polysaccharides and a potent catalyst for brain tissue regeneration and helps to improve memory and cognitive functions. Its fruiting bodies and the fungal mycelia exhibit various pharmacological activities, including the enhancement of the immune system, antitumor, hypoglycemic and anti-aging properties. H. erinaceus stimulates the synthesis of Nerve Growth Factor (NGF) which is the primary protein nutrient responsible for enhancing and repairing neurological disorders. Especially hericenones and erinacines isolated from its fruitin body stimulate NGF, synthesis. This fungus is also utilized to regulate blood levels of glucose, triglycerides and cholesterol. H. erinaceus can be considered as useful therapeutic agents in the management and/or treatment of neurodegeneration diseases. However, this review focuses on in vitro, in vivo and clinical trials for neurodegerative disease.

Neurotrophic factors are essential to maintain and organize neurons functionally; thereby neurotrophic factor-like substances or their inducers are expected to be applied to the treatment of neurodegenerative diseases such as stroke. In the present study, we firstly examined the effects of ethanol extracts of Hericium erinaceus (HE, Yamabushitake), on nerve growth factor expression in neuronal cells. HE extract promoted NGF expression in a brain tissue. Here we assessed neuroprotective effects of HE with a transient global cerebral ischemia model. Global cerebral ischemia was induced by occluding both common carotid arteries. Treatment with HE was initiated after ischemia induction and given once a day for 7 consecutive days. Neuronal cell loss in CA1 of hippocampus was significantly decreased and the performance in the Morris water maze was significantly improved in rats administered HE. We conclude that treatment with HE attenuated learning and memory deficits, motor functional disability, and neuronal cell loss induced by global cerebral ischemia. These results suggest that HE may be a potential candidate for the treatment of vascular dementia.