Research - Huperzine A

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HUPERZINE A

Huperzine A supports peak acetylcholine levels in the brain, nervous system and neuromuscular junctions.

Huperzine A

Huperzine A is a naturally occurring sesquiterpene alkaloid found in the extracts of the firmoss Huperzia serrata. The botanical has been used in China for centuries for the treatment of swelling, fever and blood disorders. Recently in clinical trials in China, it has demonstrated neuroprotective effects. It is currently being investigated as a possible treatment for diseases characterized by neurodegeneration – particularly Alzheimer’s disease.
Huperzine A has attracted the attention of Western medical science. It has been found to be an inhibitor of the enzyme acetylcholinesterase. This is the same mechanism of action of pharmaceutical drugs such as galantamine and donepezil used to treat Alzheimer’s disease.
Clinical trials in China have shown that huperzine A is comparably effective to the drugs currently on the market, and may even be a bit safer in terms of side effects. Currently, the National Institute on Aging is conducting a Phase II clinical trial to evaluate the safety and efficiency of Huperzine A in the treatment of Alzheimer’s disease in a randomized controlled trial of its effect on cognitive function. Recently, it has been investigated for its effectiveness against epilepsy in an initial 20-person clinical study by Harvard University neuroscientists examining its worth and side effects in those who are not satisfactorily treated by existing pharmaceuticals.

Tang XC, Huperzine A (shuangyiping): a promising drug for Alzheimer‚s disease. Chung Kuo Yao Li Hsueh Pao 1996 Nov;17(6):481-4. Department of Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, China. Hup A, a novel alkaloid isolated from Chineses herb Huperzia serrata, is a potent and selective inhibitor of AChE, with a rapid absorption and penetration into the brain in experimental animals. The inhibition is reversible with a longer duration of action. Hup A exhibited memory-enhancing activities in a broad range of animal cognitive model. Compared to Phy, Tac, and Gal, Hup A has better therapeutic indices, and peripheral cholinergic side effects are minimal at therapeutic doses. These findings suggest that Hup A is a promising candidate for clinical development as a symptomatic treatment for AD.

Ved HS, Koenig ML, Dave JR, Doctor BP, Huperzine A, a potential therapeutic agent for dementia, reduces neuronal cell death caused by glutamate. Neuroreport 1997 Mar 3;8(4):963-8. Division of Biochemistry, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA. Huperzine a, a potential therapeutic agent for Alzheimer‚s disease, inhibits acetylcholinesterase in primary cultures derived from forebrain, hippocampus, cortex and cerebellum of embryonic rat brain. Glutamate induces cell death in cultures from all these brain regions. Maximum cell toxicity was observed in cerebellar cultures. Pretreatment of cell cultures with Huperzine A reduced cell toxicity, as evidenced by cytotoxicity assay and general morphology. Huperzine A pretreatment also reduced glutamate-induced calcium mobilization, but did not affect elevations in intraneuronal free Ca2+ ([Ca]i) caused by KCl or (-)Bay K 8644. The data suggest that Huperzine A could be a potent neuroprotective agent not only where cholinergic neurons are impaired, but also under conditions in which glutamatergic functions are compromised.

Cheng DH, Ren H, Tang XC, Huperzine A, a novel promising acetylcholinesterase inhibitor. Neuroreport 1996 Dec 20;8(1):97-101. State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, P.R. China. The effects of huperzine A on memory impairments induced by scopolamine were evaluated using a radial maze task and inhibition of cholinesterase in vitro compared with the effects of E2020 and tacrine. Scopolamine (0.2 mg kg-1) significantly impaired spatial memory in rats. Huperzine A (0.1-0.4 mg kg-1, p.o.), E2020 (0.5-1.0 mg kg-1, p.o.) and tacrine (1.0-2.0 mg kg-1, p.o.) could reverse these scopolamine-induced memory deficits. The ratios of huperzine A, E2020 and tacrine for butyrylcholinesterase:acetylcholinesterase determined by a colourimetric method were 884.57, 489.05, and 0.80, respectively. The results demonstrated that huperzine A was the most selective acetylcholinesterase inhibitor, and improved the working memory deficit induced by scopolamine significantly better than did E2020 or tacrine, suggesting it may be a promising agent for clinical therapy of cognitive impairment in patients with Alzheimer‚s Disease.