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The Neuroprotective Properties of Hericium erinaceus in Glutamate-Damaged Differentiated PC12 Cells and an Alzheimer’s Disease Mouse Model

Summary

This research investigated how Lion’s Mane mushroom extract could protect brain cells and improve symptoms of Alzheimer’s disease. The study found that the mushroom extract helped protect brain cells from damage and improved memory and movement in mice with Alzheimer’s-like symptoms. This has important implications for everyday life: • Lion’s Mane mushroom could potentially be used as a natural supplement to help prevent or treat Alzheimer’s disease • The mushroom’s protective effects on brain cells suggest it may help maintain cognitive function as we age • As a safe, edible mushroom, it offers a natural alternative to synthetic drugs • The findings support traditional use of this mushroom for brain health • This research opens new possibilities for developing natural treatments for neurodegenerative diseases

Background

Chronic progressive degenerative damage to the central nervous system can cause neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). These conditions have drawn significant attention due to their devastating nature and limited therapeutic options. AD, an irreversible degenerative disease and the main cause of dementia, affects 60%-65% of people worldwide and frequently occurs among the elderly.

Objective

To explore the neuroprotective effects of H. erinaceus mycelium polysaccharide-enriched aqueous extract (HE) on an l-glutamic acid (l-Glu)-induced differentiated PC12 cellular apoptosis model and an AlCl3 combined with d-galactose-induced Alzheimer’s disease mouse model.

Results

HE successfully induced PC12 cell differentiation and effectively reversed the reduction of cell viability and enhancement of nuclear apoptosis rate in DPC12 cells. It suppressed intracellular reactive oxygen species accumulation, blocked Ca2+ overload and prevented mitochondrial membrane potential depolarization. In AD mice, HE enhanced horizontal and vertical movements, improved endurance time in rotarod tests, and decreased escape latency time in water maze tests. It also improved central cholinergic system function by enhancing acetylcholine and choline acetyltransferase concentrations in both serum and hypothalamus.

Conclusion

HE protects DPC12 cells against l-Glu-induced neurotoxicity primarily through mitochondria-related pathways. The protective effects were confirmed in AlCl3- and d-gal-induced AD mice, likely involving the modulation of neurotransmitters. These findings provide experimental evidence that HE may serve as a neuroprotective candidate for treating or preventing neurodegenerative diseases.
  • Published in:International Journal of Molecular Sciences,
  • Study Type:Experimental Study,
  • Source: 10.3390/ijms17111810
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