The following report about Huperzine-A is from the American Academy of Neurology, The most widely read and highly cited peer-reviewed neurology journal.
Huperzine A is a natural cholinesterase inhibitor derived from the Chinese herb Huperzia serratathat may compare favorably in symptomatic efficacy to cholinesterase inhibitors currently in use for Alzheimer disease (AD).
Huperzine A is an alkaloid extract of the plant Huperzia serrata that may be useful as a treatment for Alzheimer disease (AD). During the 1980s, investigators in China determined that huperzine A is a potent inhibitor of acetylcholinesterase (AChE),1 a finding that has been confirmed repeatedly.2,3 It is highly selective for AChE in vitro, it has good brain penetration, and it is relatively free of cholinergic toxicity.4–6 In addition, some studies have shown that huperzine A may shift amyloid precursor protein (APP) metabolism toward the nonamyloidogenic α-secretase pathway.7 Based on the 50% inhibitory concentration (IC50), huperzine A is more potent than tacrine, physostigmine, and galantamine with respect to inhibition of AChE activity. Hence, it is presumed that huperzine A, if efficacious, would exert its clinical efficacy in AD via this mechanism. Certainly, it should be noted that huperzine has been shown to exhibit other effects that may be beneficial AD: huperzine has been demonstrated to reduce glutamate-induced cytotoxicity by antagonizing cerebral NMDA receptors.8 Importantly, this trial was designed to assess short-term symptomatic effects more likely attributable to AChEI or memantine-like effects than to neuroprotective mechanisms.
A total of 210 patients were enrolled in this study. The protocol was reviewed and approved by the institutional review board at each participating site. All research participants and caregivers gave written informed consent. Surrogate consent was used if criteria were met for its use. The Alzheimer's Disease Cooperative Study's Data and Safety Monitoring Board, which is advisory to the National Institute of Aging, provided safety oversight on an ongoing basis. The clinical trial identifier number for this study was NCT00083590. Blinded phase enrollment began June 2004 and last week 24 visit December 2007.
The present study represents an initial attempt to characterize the impact of short-term huperzine A treatment on individuals with mild to moderate AD. The primary endpoint for this trial, cognitive benefit as indicated by the change in ADAS-Cog score for the 200 μg BID dose at 16 weeks compared to placebo, did not indicate efficacy; we therefore cannot conclude that huperzine A provides cognitive enhancement in mild to moderate AD. However, the 200 μg BID did favorably influence MMSE scores at 16 weeks, and the 400 μg BID dose showed evidence of cognitive enhancement as measured by the ADAS-Cog and the MMSE. Thus, the results suggest a possible short-term symptomatic benefit of huperzine A, which requires confirmation in additional studies. Huperzine was generally well-tolerated at both doses tested.
Read more about about this trial at the link below