Huperzine Benefits

Huperzine A may be used to treat dementia, memory loss, and other cognitive deficiencies. It may also be helpful for individuals with myasthenia gravis and it may protect against poisoning with organophosphate chemicals.

Studies carried out in China indicated that Huperzine A, is a promising new treatment for Alzheimer’s disease. Other studies indicate that Huperzine A is a superior acetylcholine esterase (AChE) inhibitor with excellent penetration into the CNS and a remarkable in vivo half-life. Two double-blind clinical trials carried out in China demonstrate that Huperzine A is both safe and effective for the long term treatment of Alzheimer's dementia. In addition to its activity as an AChE inhibitor, recent findings suggest that Huperzine A has other neuroprotective functions:

1) Huperzine A inhibits glutamate-induced cytotoxicity in cultures of rat neonatal hippocampal and cerebella neurons;

2) Huperzine A promotes dendrite outgrowth of neuronal cultures.

Alzheimer’s disease is characterized by abnormalities and degeneration of neurons which depend upon acetylcholine and acetylcholine esterase for normal activity and viability. These cells located in the basal forebrain are also implicated in other neurological diseases such as Parkinson’s disease. Huperzine A is a potent inhibitor of acetylcholine esterase, superior in activity to TACRINE, the first drug licensed in the USA for Alzheimer’s disease and E2020 which was licensed recently by Eisai Pharmaceuticals. In addition, Huperzine A has been shown to protect neuronal cells in culture from death caused by the excitoamino acid glutamate.

Huperzine A has been proven superior to drugs licensed for the treatment of Alzheimer’s, including the leading anticholinesterase drugs physostigmine and tacrine. Huperzine A improved learning and memory in mice better than tacrine. Unlike physostigmine and tacrine, Huperzine A acts specifically on AchE in the brain rather than AchE found elsewhere in the body—i.e., far less is wasted on irrelevant effects. Unlike physostigmine and tacrine, Huperzine A does not appear to bind to receptors in the central nervous system, which can cause adverse side effects. Its effects last 10 to 12 times longer than physostigmine and tacrine (up to 8 hours).

Studies show Huperzine inhibits AchE, the enzyme that destroys acetylcholine, and thereby strengthens or lengthens the duration of the nerve impulse. This alone could make the difference between vaguely remembering something and clear recollection.

Additional studies have found Huperzine A to decrease neuronal cell death caused by toxic levels of glutamate. This finding may make Huperzine A a potential therapy for reducing neuronal injury from strokes, epilepsy, and other disorders. HupA has been used in China for several years in the treatment of dementia. Reports from an estimated 100,000 people treated, suggest low toxicity for this drug.