Manthis F. (Sang Piao Xiao San): Kidney Qi Xu (Deficiency) with Heart Qi Xu (Deficiency): absentmindedness, forgetfulness, frequent urination
(Hsu, 1980, p. 361; Yeung, p. 192; Bensky and Barolet, p. 362)
Shou Wu Pian (patent): Liver Yin Xu (Deficiency) with Kidney Yin Xu (Deficiency) and Xue Xu (Blood Deficiency) (Naeser, p. 296)
Gui Ling Ji (patent): Kidney Yang Xu (Deficiency) (Zhu, p. 297)
Bu Nao Wan (patent): Heart Xue Xu (Blood Deficiency) with Liver Wind Stirring: dizziness (Zhu, p. 316)
An Mian Pian (patent): Heart Yin Xu (Deficiency) with False Fire: agitation (Zhu, p. 327)
Eleuthero 10+ (patent): Kidney Jing Xu (Essence Deficiency) (Dharmananda, 1990, p. 14)
» research: Huperzine A , an alkaloid isolated from the moss Huperzia serrata, has been found to enhance memory in Alzheimer's patients by preventing the breakdown of acetylcholine by inhibiting acetylcholinesterase, the enzyme responsible for breaking down acetylcholine. The enhanced levels of acetylcholine in brain cells contributes to improved spatial working memory and cognitive function. The medication is significantly less toxic than conventional acetylcholinesterase-inhibitors, such as physostigmine, Tacrine and Donepezil; research to this point has found no serious side effects after wide use for almost a decade. In one double-blind clinical study, 200 mcg of Huperzine A, twice daily, produced measurable improvements in memory, cognitive function, and behavioral factors in 58% of Alzheimer's patients. (Xu SS, et al. Chung Kuo Yao Li Hsueh Pao 1995 Sep;16(5):391-395.)
footnotes
Hanin I, Tang XC, Kindel GL, Kozikowski AP. Natural and synthetic Huperzine A: effect on cholinergic function in vitro and in vivo. Ann N Y Acad Sci 1993 Sep 24;695:304-306.
Abstract: Huperzine A has been shown to be useful in the treatment of symptoms of dementia of the Alzheimer type. Our initial attempts to synthesize (-)Huperzine A resulted in the racemic mixture of (+/-)Huperzine A. We have therefore compared the in vitro and in vivo effects of (+/-)Huperzine A with those of (-)Huperzine A in rats. The results indicate a similar biological mechanism of action between the two, but that the racemic mixture of (+/)Huperzine A has a weaker biological activity than the natural product (-)Huperzine A, presumably due to the presence in the mixture of (+)Huperzine A, which is considerably less potent than the (-)isomer.
Patocka J. Huperzine A--an interesting anticholinesterase compound from the Chinese
herbal medicine. Acta Medica (Hradec Kralove) 1998;41(4):155-157.
Abstract: Huperzine A, alkaloid from the Chinese herbal medicine Qian Ceng Ta, which is prepared from the moss Huperzia serrata, has been used in China for centuries to treat fever and inflammation. Huperzine A is a strong inhibitor of cholinesterases with high selectivity to acetylcholinesterase and in China is developed as therapeutic against Alzheimer's disease. May be that huperzine A will be better than other centrally active anticholinesterases in treating this neurodegenerative disorder. Huperzine A appears to have additional pharmacological properties that make it an attractive candidate therapy for clinical
trials.
Skolnick AA. Old Chinese herbal medicine used for fever yields possible new Alzheimer
disease therapy. JAMA 1997 Mar 12;277(10):776.
Tang XC. Huperzine A (shuangyiping): a promising drug for Alzheimer's disease. Chung Kuo Yao Li Hsueh Pao 1996 Nov;17(6):481-484.
Abstract: 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):963-968.
Abstract: 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.
Xu SS, Gao ZX, Weng Z, Du ZM, Xu WA, Yang JS, Zhang ML, Tong ZH, Fang YS, Chai XS, et al. Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimer's disease. Chung Kuo Yao Li Hsueh Pao 1995 Sep;16(5):391-395.
Abstract: AIM: To evaluate the efficacy and safety of tablet huperzine-A (Hup) in patients with Alzheimer's disease. METHODS: Using multicenter, prospective, double-blind, parallel, placebo controlled and randomized method, 50 patients were administered orally 0.2 mg (4 tablets) Hup and 53 patients were given po 4 tablets of placebo twice daily for 8 wk. All patients were evaluated with Wechsler memory scale, Hasegawa dementia scale, mini-mental state examination scale, activity of daily living scale, treatment emergency symptom scale, and measured with BP, HR, ECG, EEG, ALT, AKP, BUN, Cr, Hb, WBC, and urine routine. RESULTS: About 58% (29/50) of patients treated with Hup showed improvements in their memory (P < 0.01), cognitive (P < 0.01), and behavioral (P < 0.01 functions. The efficacy of Hup was better than placebo (36%, 19/53) (P < 0.05). No severe side effect was found. CONCLUSION: Hup is a promising drug for symptomatic treatment of Alzheimer's disease.
Ye JW, Cai JX, Wang LM, Tang XC. Improving effects of huperzine A on spatial working memory in aged monkeys and young adult monkeys with experimental cognitive impairment. J Pharmacol Exp Ther 1999 Feb;288(2):814-819.
Abstract: Our previous studies demonstrated that huperzine A, a reversible and selective acetylcholinesterase inhibitor, exerts beneficial effects on memory deficits in various rodent models of amnesia. To extend the antiamnesic action of huperzine A
to nonhuman primates, huperzine A was evaluated for its ability to reverse the deficits in spatial memory produced by scopolamine in young adult monkeys or those that are naturally occurring in aged monkeys using a delayed-response task. Scopolamine, a muscarinic receptor antagonist, dose dependently impaired performance with the highest dose (0.03 mg/kg, i.m.) producing a significant reduction in choice accuracy in young adult monkeys. The delayed performance changed from an average of 26.8/30 trials correct on saline control to an average of 20.2/30 trials correct after scopolamine
administration. Huperzine A (0.01-0. 1 mg/kg, i.m.) significantly reversed deficits induced by scopolamine in young adult monkeys on a delayed-response task; performance after an optimal dose (0.1 mg/kg) averaged 25.0/30 correct. In four aged monkeys, huperzine A (0.001-0.01 mg/kg, i.m.) significantly increased choice accuracy from 20.5/30 on saline control to 25.2/30 at the optimal dose (0.001 mg/kg for two monkeys and 0.01 mg/kg for the other two monkeys). The beneficial effects of huperzine A on delayed-response performance were long lasting; monkeys remained improved for about 24 h after a single injection of huperzine A. This study extended the findings that huperzine A improves the mnemonic performance requiring working memory in monkeys, and suggests that huperzine A may be a promising agent for clinical therapy of cognitive impairments in patients with Alzheimer's disease.