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Huperzine A and the Brain

Chip Engelmann

Huperzine A is a derivative of the extract of club moss. Club moss grows at high elevation and in cold climates of China. Also known as Qian Ceng Ta, the herb has been used to treat fever, inflammation and dementia. More recently, Huperzine A was found to be beneficial for learning and memory retention, improved focus and attention, improved nerve transmission to muscles, and for dementia resulting from stroke, senile or presenile dementia, and Alzheimer's disease. Huperzine A was first isolated by the Chinese Academy of Sciences in 1986 and was first synthesized by an American, Dr. Alan Kozikowski of Georgetown, in 1997.

According to Dr. Bebasis Bagchi and Jean Barrilla, "Alzheimer's disease is a progressive, degenerative disease that attacks the brain and results in impaired memory, thinking and behavior...This mental decline is related to a loss of nerve cells and the links or synapses between them. Alzheimer's disease is the most common form of dementia. It is not part of the aging process and always represents a disease process." Alzheimer's disease is the fourth leading cause of death in adults after heart disease, cancer and stroke. Huperzine A improves mental demise by inhibiting the breakdown of acetylcholine.

They go on to say, "Acetylcholine is the neurotransmitter in the brain that is responsible for carrying electrical impulses from one nerve to another. It is made in the...nerve fibers and packaged into small vesicles where it is stored until released. Once acetylcholine has been secreted by the nerve ending, it persists only for a few seconds. In a normal brain, the enzyme acetylcholinesterase serves a housekeeping function by breaking down acetylcholine...The choline is transmitted back to the nerve endings to be used again to make acetylcholine." The brains of people with Alzheimer's are deficient in acetylcholine because of damage to the nerve cells that secrete it. Unfortunately, acetylcholinesterase keeps working to get rid of whatever acetylcholine is released from the damaged nerve cell, compounding the deficiency. Huperzine A stops this enzyme from breaking down the acetylcholine, thus allowing acetylcholine to build up and improve mental function.





Copyright (c) 2001 by Chip Engelmann