Huperzine A is commonly found in brain supplements and is used to enhance short-term memory associated with aging and is taken by many individuals who have Alzheimer’s disease. Huperzine A is also used by students to boost their memory while studying for exams. It has also been used to treat inflammation, fever and various blood disorders for centuries in Asia.

The molecule is isolated from the Chinese club moss and has been scientifically studied in China and the United States. Huperzine A binds to the enzyme acetylcholinesterase found in the synaptic cleft between neurons and inhibits it thereby protecting the neurotransmitter acetylcholine responsible for short-term memory. By allowing the transmitter acetylcholine to remain around longer in the synaptic cleft, mental concentration, focus and attention are enhanced boosting memory ability.

This is particularly important for Alzheimer’s patients that have difficulty remembering what they are doing from one moment to the next. This allows enough transmitter to hang around long enough to increase signal transduction that can make the difference in being able to perform simple tasks like eating, getting dressed, washing dishes, taking a bath or remembering what someone said a moment ago.

Acetylcholinesterase is an enzyme that contains what is called an active site that binds the substrate acetylcholine.

This site actually breaks down acetylcholine into acetate and choline which deactivates the neurotransmitter so it can no longer bind to its receptors on the post synaptic cell. This stops signal transduction. This enzyme also has what is called an allosteric site that binds an inhibitor. When an inhibitor binds it alters the shape of the active site preventing binding of the enzyme’s substrate (acetylcholine). In this case, Huperzine A binds to the allosteric site closing off the active site so that acetylcholine can’t bind therefore allowing acetylcholine to remain in the synaptic cleft longer.

This allows acetylcholine to bind and rebind to its receptors on the postsynaptic cell ensuring a strong signal to be generated in the post synaptic neuron. This can make up for a decline in the amount of acetylcholine that is released into the synaptic cleft due to damaged neurons from general aging and neuronal abnormalities caused by Alzheimer’s disease. In Alzheimer’s disease, excess proteins build up in the neuronal cell body and axons forming neurofibrillary tangles and amyloid plaque.

The neuronal cell body and axon become abnormally shaped and eventually the axon will break into segments and lose connection with their own cell body. As the cholinergic cells become irregularly shaped the axons pull away from neurons they are talking to.

At this point, the neurotransmitter (acetylcholine) is released intermittently and in low concentration until the axons are completely fragmented into pieces and can no longer release transmitter. Scientific studies have demonstrated that in the early stages of Alzheimer’s disease. oral administration of Huperzine A inhibits acetylcholinesterase activity thereby enhancing or boosting the decrease in the amount of acetylcholine being released by inhibiting the transmitter’s breakdown. Thus providing for enough signal to carry short-term memory function allowing an individual to remember what is currently going on from moment to moment.