|
How Huperzine Works 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.
| 
