Some researchers think the moss Huperzia serrata, a Chinese herb known as Qian Ceng Ta, may prove to be a better treatment for Alzheimer disease (AD) than the two drugs currently on the market. Although this herb was used to treat fever and inflammation for centuries in China, it does not have antipyretic or anti-inflammatory properties. According to laboratory and x-ray crystallography studies, the alkaloid compound Huperzine A found in H. serrata does appear to be a strong acetyl-cholinesterase (AChE) inhibitor.

Acetylcholine is a neuro-transmitter that makes communication between neurons, or nerve cells, possible. Ordinarily, AChE cleans up neuronal synapses (the point of contact between two neurons) by breaking down excess acetylcholine. AChe quickly breaks down acetylcholine produced in the brains of AD patients, resulting in memory loss and other cognitive defects. AChE inhibitors work by preventing the breakdown of acetylcholine.

Huperzine A appears to bind more tightly and specifically to AChE than tacrine and donepezil, the current drugs for treatment of AD. HuperzineA also has a longer half-life and a slower rate of dissociation, characteristics that make it a more effective therapy. Tacrine and donepezil produce cholinergic side effects in many patients, such as nausea, vomiting, salivation, and sweating. Tacrine can also cause liver damage. Studies suggest that HuperzineA may be more effective with fewer adverse effects than tacrine or donepezil.

Alzheimer's disease is a neurodegenerative disorder associated with neuritic plaques that affect the cerebral cortex, amygdala and hippocampus. There is also neurotransmission damage in the brain. One of the major functional deficits in Alzheimer's disease is a hypofunction of cholinergic neurons. This leads to the cholinergic hypothesis of Alzheimer's disease and the rationale for strategies to increase acetylcholine in the brains of Alzheimer's disease patients. Two FDA-approved drugs for the treatment of Alzheimer's disease, tacrine and donepezil, are acetylcholinesterase inhibitors.

Huperzine A is also an acetylcholinesterase inhibitor and has been found to increase acetylcholine levels in the rat brain following its administration. It also increases norepinephrine and dopamine, but not serotonin levels. The natural L or (-)-Huperzine A is approximately three times more potent than the racemic or (±)-Huperzine A in vitro.

Researchers believe Huperzine works by protecting a key neurotransmitter called acetylcholine. Acetylcholine is released at the synapse (gap) between two nerve cells and stimulates the impulse from one brain cell to the next. An enzyme called acetylcholine esterase (AchE) then destroys the acetylcholine and terminates the nerve signal (after it’s been transmitted). Scientists believe that in some memory disorders the acetylcholine is destroyed too soon, and the nerve impulse is too weak to be received—an undesirable effect that may also play a role in normal, age related memory deficits.