Galantamine Can Improve Your Quality of Life

Galantamine Helps Save
Memory, and Money Too

The secret lies in what galantamine can do that its rivals can't do

e're always looking for an edge - something that gives us a special advantage. It's human nature. Consider the humble chair: it serves only one purpose (OK, two, if you happen to be a lion tamer): you sit on it. It doesn't matter which of the zillion different designs that chair has, it's still just a chair. Then some genius looks at chairs in a new way, says, "I can do better than that," and invents the BarcaLounger.

Instant edge! People flock to it. They don't just sit on it, they lounge on it. Although it doesn't make ordinary chairs obsolete, it sets a new standard that no previous chairs can match, because it can do something they can't do.

Galantamine is like that. It's not just an acetylcholinesterase inhibitor (a what?), but an acetylcholinesterase inhibitor that's better than the others, in part because it can do something they can't do: it can modulate nicotinic receptors in the cholinergic system, making it more effective in combating Alzheimer's disease than drugs such as donepezil and rivastigmine.

Sorry! If you choked on some of the terms we just threw at you, fear not - we'll explain them. For starters, galantamine is an alkaloid extracted (at considerable cost, by the way) from flowers such as the snowdrop (Galanthus nivalis), the daffodil (Narcissus pseudonarcissus L.), and the spider lily (Lycoris radiata). It has a long history of use, going back many centuries, for a variety of medicinal purposes, particularly the alleviation of neuromuscular ailments such as neuritis and neuralgia.

In modern times, scientific interest in galantamine has focused on its benefits for treating jet lag,1 fatigue syndrome,2 and even impotence.3 By far the greatest interest, however, is devoted to galantamine's use in treating Alzheimer's disease, because of its exceptional qualities as an acetylcholinesterase inhibitor (AChEI).4 That means that it's a substance that inhibits the biochemical action of acetylcholinesterase (AChE). And that's good.

Acetylcholinesterase is an enzyme that destroys acetylcholine (ACh). That's bad (relatively speaking). ACh, as you may know, is one of the body's and brain's most important neurotransmitters - a carrier of nerve impulses across the tiny gaps, called synapses, between one nerve cell (neuron) and the next. ACh facilitates memory, among other things. That's good.

Did you follow that good/bad/good sequence? OK, think of it again, in reverse, like this: ACh is good because it's a vital neurotransmitter and is crucial to memory. AChE is bad because it destroys ACh (not all of it, just some of it). And galantamine is good because it inhibits AChE from doing that (which makes galantamine an AChEI). It's like the old saying, "The enemy of my enemy is my friend." To anyone facing the prospect of Alzheimer's disease, there is probably no greater friend than galantamine. Let's see why that’s true.

The part of the nervous system for which acetylcholine acts as the sole or primary neurotransmitter - and that means the great majority of the entire nervous system, peripheral as well as central - is called the cholinergic system. In this article, our interest is in the brain portion of the cholinergic system, because that is where Alzheimer's disease strikes. And where Alzheimer's strikes, galantamine - better than anything else - acts to thwart it.

Alzheimer's disease, the most prevalent form of dementia, is due in part to a deficiency of acetylcholine in certain parts of the brain. This robs its victims of memory and other vital aspects of cognitive function, including the ability to perform many of the mundane tasks of daily living. It can also rob them of several years of their life, as a recent Canadian study has shown.5

Whenever ACh deficiency is mentioned, one thinks right away of AChE, the enzyme that destroys ACh. It's not that AChE is intrinsically bad - on the contrary, it's absolutely essential for good health and for life itself - but that its effect can be bad if it gets the upper hand in the never-ending balancing act between itself and ACh. In the exquisite biochemistry of the brain, ACh is constantly being formed in the synapses and is just as constantly being "mopped up" by AChE.

The incentive to find better
acetylcholinesterase inhibitors is
tremendous. And that's where
galantamine comes in.

If AChE does manage to gain the upper hand, we want to restore the balance by using an AChEI (acetylcholinesterase inhibitor, remember?). This is, in fact, the only significant pharmacological intervention used for Alzheimer's disease in modern medical practice. The incentive to find better AChEIs, therefore, is tremendous. And that's where galantamine comes in.

Galantamine doesn't destroy AChE (if it did that, there would be havocin our brains). It just slows it down some, thereby giving ACh levels a boost - a much-needed boost if they are low because of Alzheimer's disease or any other form of age-related cognitive impairment. So far, so good. But other AChEIs can do that too. The two that are most commonly used for Alzheimer's are the prescription drugs donepezil and rivastigmine (the drug tacrine is rarely prescribed any more, owing to its severe side effects, especially liver damage).

Now we've explained all the terms in that "choker" paragraph except one: nicotinic receptors. We saved the best for last, because this is where galantamine gains its special edge, by doing something that donepezil and rivastigmine can't do: galantamine modulates nicotinic receptors (we'll explain them in a moment), thereby enhancing the effectiveness of acetylcholine as a neurotransmitter.6,7

Figure 1.
A nerve impulse consists of an electric current in one neuron being "forwarded" to a neighboring neuron by means of a chemical signal - the release of neurotransmitter molecules - between them.

Here's how it works. A nerve impulse, in the form of a tiny electric current, propagates down the length of a neuron. (Don't get us started on how that impulse got started - there's only so much we can cover in one article.) When it reaches the end, it causes a swarm of acetylcholine molecules to be released into the synapse (see Figure 1). As the molecules diffuse across that tiny gap, their "mission" is to stimulate the ending of the neuron they're approaching, thereby initiating another tiny electric current that will propagate down the length of that neuron to the next synapse, and so on until the signal reaches its destination.

Galantamine's ability to make
more acetylcholine available
and to make the acetylcholine
receptors more sensitive is
why it is so effective against
Alzheimer's disease.

But how does a neurotransmitter stimulate a nerve ending? The answer lies in receptor sites. These are highly specialized protein complexes that dot the surface of the nerve ending, waiting for neurotransmitter molecules to show up and "turn them on," with literally electrifying results. The receptors are sensitive only to their particular kind of neurotransmitter or to molecules that mimic them.

Sometimes, however, other molecules can modulate the properties of receptor sites, through chemical interactions, in such a way as to make them even more sensitive to their designated neurotransmitter. When that occurs, nerve impulses travel more surely and efficiently, and cognitive function is enhanced.

For acetylcholine molecules, there are two main kinds of neuronal receptors: nicotinic receptors and muscarinic receptors. We'll spare you the details; suffice it to say that the nicotinic receptors (so named because they are very sensitive to the brain-stimulating nicotine molecule) can be modulated - sensitized, if you will - by galantamine. Neither donepezil nor rivastigmine, however, has that capability.

How Galantamine Can Save Money
Associated with every disease are significant costs. There are financial burdens, of course, but also the loss of emotional well-being, and the toll that that can take on one's family and friends, as well as one's self. This is particularly true of dementias, such as Alzheimer's, whose insidious action erodes their victims' personalities by robbing them of their life's memories and even of their sense of who they are. It is an awful thing to endure, or to witness.

As the disease progresses and cognitive functions deteriorate, patients need more and more physical care to get through the day. Eventually they may become so dependent that full-time care is required. The financial cost of that, of course, is great. Thus it is useful to evaluate the extent to which therapy can delay the time when full-time care becomes necessary. A further consideration is the extent to which the level of that care, and thus its cost, can be reduced through the beneficial effects of ongoing therapy - taking the cost of the therapy itself into account, of course.

A study of the use of galantamine therapy (24 mg per day) compared with no pharmacological therapy has addressed these questions for Canadian patients with mild to moderate Alzheimer's disease.1 Using data from two prior placebo-controlled clinical trials of 6 months duration,2,3 the researchers went to great lengths to devise reasonable assumptions and equations upon which to base computations of probable long-term costs over a 10-year period.

To make a long and complicated story short, the computer model devised for this study predicted that galantamine therapy would reduce the duration of full-time care by almost 10% over the 10-year period. When all patients were considered in the computations, the savings per patient averaged $US528. When only those patients with moderate Alzheimer's were considered, however,the savings were much greater, rising to $US2533.

The model results also predicted that patients treated with galantamine were likely to remain at home longer, and thus spend less time in nursing homes. These results were sustained over a broad range of input parameters.

The researchers concluded that "Galantamine cannot only potentially increase the time before patients require full-time care, but may also lead to overall savings because treatment costs are offset by reductions in other health care expenditures."


  1. Getsios D, Caro JJ, Caro G, Ishak K. Assessment of health economics in Alzheimer's disease (AHEAD): galantamine treatment in Canada. Neurology 2001;57:972-8.
  2. Raskind MA, Peskind ER, Wessel T, Yuan W, and the Galantamine USA-1 Study Group. Galantamine in Alzheimer's disease: a 6-month, randomized, placebo-controlled trial with a 6-month extension. Neurology 2000;54:2261-8.
  3. Wilcock GK, Lilienfeld S, Gaens E, on behalf of the Galantamine International-1 Study Group. Efficacy and safety of galantamine in patients with mild to moderate Alzheimer's disease: a multicenter, randomized, controlled trial. Br Med J 2000;321:1-7.

The importance of this aspect of galantamine's action is underscored by the fact that, with advancing age, our nicotinic receptors tend to decrease both in number and in sensitivity. Thus, galantamine's ability not only to make more ACh available, by inhibiting AChE, but also to make the ACh receptors more sensitive to the neurotransmitters, represents a unique bonus. And that is why galantamine is the most effective AChEI currently in use against Alzheimer's disease.

New evidence of galantamine's value comes from a randomized, double-blind, placebo-controlled trial to evaluate the efficacy and tolerability of galantamine taken at three different dosages - 18, 24, and 36 mg per day - for 3 months.8 The subjects were 285 patients (males and females over 45 years of age, with an average age of 74) divided into four groups: one for each of the three dosages, plus a control group.

All the subjects had mild to moderate Alzheimer's disease, and they were screened to exclude those who had dementia that might be due to any other cause, such as vascular dementia.* Also excluded were those who were taking any kind of drug that might cloud the interpretation of the results, such as antidepressants, antipsychotics, sedatives, and most antihypertensives.

*Although one would not expect galantamine to be effective against vascular dementia, which arises from cerebrovascular disease - a different process than whatever it is that causes Alzheimer's disease (no one really knows) - there is some evidence that it is effective. (See "Galantamine Beats Prescription Drugs for Combating Mental Decline," Life Enhancement, September 2001.)

The researchers evaluated the patients' condition at baseline (the beginning of the study) and again after 6 and 12 weeks, by means of standardized tests of cognitive function and activities of daily living (the latter can be used as indicators for an overall quality-of-life assessment). They found that at all dosages, galantamine significantly improved the patients' condition, with the greatest gains being realized at the intermediate, 24-mg dose (demonstrating yet again that more is not always better).

The computer model predicted
that patients treated with
galantamine were likely to
remain at home longer, and
thus spend less time in
nursing homes.

The authors concluded that ". . . the favorable effects of galantamine on patients' quality of life confirm that its effects on cognitive function are clinically relevant." In their opinion, the 24-mg dose is optimal for the treatment of Alzheimer's disease, based on both the efficacy and tolerability results. This view is supported by a previous, long-term study showing that 24 mg per day of galantamine preserves patients' cognitive and functional abilities at baseline levels for at least 12 months.9 The present authors point out, however, that 16 mg per day may be adequate for some people.

One feature of the study's design is especially worth noting for anyone who might be contemplating the use of galantamine as a dietary supplement. Although the study lasted for 12 weeks, the patients did not receive the full dosages of galantamine for that entire period. With galantamine it is preferable to start small and build to the desired dosage gradually, so as to allow the body to adjust to its new condition and to minimize potential side effects.

In the study, the patients started by taking 4 mg of galantamine twice daily. The dosages were increased at 2-to-3-day intervals until the target levels of 6, 8, and 12 mg three times daily were reached (after 5, 8, and 14 days, respectively). This dose-escalation period was followed by 10 weeks of full dosage for all the patients.

Overall, the galantamine was well tolerated, although the authors admitted that the fairly short dose-escalation period of 1-2 weeks may have affected the tolerability adversely, especially in the highest-dose group. Side effects of the treatment, consisting mainly of mild and transient nausea and other symptoms of gastrointestinal upset, occurred mainly during the dose-escalation period. Thereafter the incidence of side effects declined rapidly to levels similar to those associated with placebo.

At all dosages, galantamine
significantly improved the
patients' condition, with the
greatest gains being realized at
the intermediate, 24-mg dose.

Laboratory tests showed no clinically relevant changes. In particular, there were no indications of liver damage (and there never have been in any studies with galantamine). Liver damage used to be a major concern in Alzheimer's therapy when tacrine was used, but that has become a nonissue, because none of the Alzheimer's drugs now in common use cause liver damage.

Fortunately for American consumers, galantamine is available in the United States without a prescription, even though it was brought to market as a prescription drug in 2001, under the name Reminyl®.Whats more;high-purity galantamine is available unlike Reminyl, augmented with the acetylcholine precursor choline, together with choline's vital cofactor, pantothenic acid (vitamin B5).

Such a formulation enhances acetylcholine levels both directly, by stimulating its production, and indirectly, by protecting what is already there. And, as we have seen, it does what other acetylcholinesterase inhibitors can't do: it enhances the efficiency of acetylcholine use in the brain by modulating those nicotinic receptors. So don't just sit there. Get up off your BarcaLounger and get some Galantamine. As supplements go, it could become your best friend.


  1. Davis BM. Method for alleviating jet lag. US Patent 5,585,375, issued Dec. 17, 1996.
  2. Snorrason E. Treatment of fatigue syndrome. US Patent 5,312,817,issued May 17, 1994.
  3. Katz R. Method of treating physiologic male erectile impotence. US Patent 5,177,070, issued Jan. 5, 1993.
  4. Olin J, Schneider L. Galantamine for Alzheimer's disease (Cochrane review). In The Cochrane Library, Issue 2, 2001. Oxford: Update Software.
  5. Wolfson C, Wolfson DB, Asgharian M, M'Lan CE, Østbye T, Rockwood K, Hogan DB. A reevaluation of the duration of survival after the onset of dementia. N Engl J Med 2001 Apr 12;344(15):1111-6.
  6. Maelicke A, Samochocki M, Jostock R, Fehrenbacher A, Ludwig J, Albuquerque EX, Zerlin M. Allosteric sensitization of nicotinic receptors by galantamine, a new treatment strategy for Alzheimer's disease. Biol Psychiatry 2001;49:279-88.
  7. Coyle J, Kershaw P. Galantamine, a cholinesterase inhibitor that allosterically modulates nicotinic receptors: effects on the course of Alzheimer's disease. Biol Psychiatry 2001;49:289-99.
  8. Wilkinson D, Murray J, in collaboration with the Galantamine Research Group. Galantamine: a randomized, double-blind, dose comparison in patients with Alzheimer's disease. Int J Geriatr Psychiatry 2001;16:852-7.
  9. Raskind MA, Peskind ER, Wessel T, Yuan W, and the Galantamine USA-1 Study Group. Galantamine in Alzheimer's disease: a 6-month, randomized, placebo-controlled trial with a 6-month extension. Neurology 2000;54:2261-8.

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