Boost Memory and Keep It
  by Will Block

In a recent issue of FEBS Letters (Federation of European Biochemical Societies), researchers at Israel's respected Weizmann Institute published an elucidation of the mechanism by which galantamine - a compound extracted from the common snowdrop (Galanthus nivalis) - blocks the action of a key brain enzyme involved in Alzheimer's disease.1 The researchers studied galantamine in detail and found that it seems to achieve the same effect as drugs such as Aricept or tacrine, but that it may go well beyond them.  

Alzheimer's disease is a severe degenerative disorder that causes memory loss and other cognitive deficits in as many as 10 percent of the elderly. A hallmark of this ominous and pervasive age-related decline is the deterioration of nerve cells that release acetylcholine, a neurotransmitter that is needed to shuttle messages in the form of electrochemical impulses within the brain. In the absence of adequate messaging, severe, age-related cognitive decline such as Alzheimer's eventually results in the reduced synthesis of proteins related to the growth of neuronal structures.2

Adding insult to injury, all the while that the release of acetylcholine (ACh) is being compromised by degenerating nerve cells, the enzyme acetylcholinesterase (AChE) is cleaving acetylcholine molecules in two at the rate of about 20,000 molecules per AChE molecule per second. Even if AChE activity declines with age, as seems to be the case, the real issue is the balance between acetylcholine production, release, and breakdown. For example, if ACh breaks down faster than it's produced and released, or if its production and release are substantially diminished, even if the rate of breakdown is not, then in these cases (and others), the result is a cholinergic dysfunction (cholinergic means pertaining to actions mediated by acetylcholine), and one's memory declines.3

The decline of acetylcholine production and release is relevant not only to Alzheimer's disease but also to dementia and other age-related memory impairments (ARMIs). Because Alzheimer's and other cognitive impairments steal away the "light" of memory, they may be thought of as "ARMIs of the night."

Using x-ray crystallography, the Weizmann Institute researchers found that galantamine binds to AChE in such a way as to destroy its ability to cleave ACh, thus putting the brakes on the depletion of these vital, memory-enhancing messenger molecules. By preserving more ACh molecules, galantamine permits the better maintenance of memory function.

Moreover, as the researchers found, galantamine does something else that none of the drugs or other herbs used to treat cholinergic decline do: it binds to acetylcholine receptors (proteins on the surface of the nerve cell that are activated by acetylcholine), thus directly stimulating neuronal function. More recent research indicates that this involves nicotinic receptors, in particular.  This is a class of specialized ACh receptors that are activated by nicotine (which is known to enhance cerebral blood flow and cognitive and psychomotor functions),* but also by various other substances, among which galantamine is one of the most potent.

Nicotinic receptors play an important role in memory and learning, and their progressive loss is one of the distinctive neuroanatomical symptoms of Alzheimer's. Another symptom is the buildup of a deleterious substance called amyloid.  It is significant that the stimulation of nicotinic receptors may be associated with an inhibition of amyloid, thus perhaps helping to preserve or recover memory.4

In terms of biological evolution, acetylcholine is an ancient compound, having occurred very early in the lower species of life, both plant and animal.5  It is thought that non-neuronal (vegetative) acetylcholine first appeared in the Precambrian era, as far back as 3 billion years ago.  Its appearance in animals is dated to approximately 500-400 million years ago, in the Paleozoic era.

Clearly, acetylcholine has played an important role in the evolution of living things, including us.  This role is not confined, however, to the realm of the mind - nor, therefore, is that of galantamine, acetylcholine's "protector."

In lower animals as well as in humans, acetylcholine is the "universal neurotransmitter" for the neuronal activation of muscle fibers.  Small wonder, then, that larger amounts of it can yield benefits for the body, as has been reported in the scientific literature.  Thus it is especially interesting to note that when galantamine was rediscovered by European scientists in the 1950s, it was found to be in folk-medicine use for neuromuscular relief, not for memory enhancement.

In the 1960s, the snowdrop (a flowering plant) was discovered to be in use in Italy for muscular soreness.6 Indeed, its earliest modern clinical use was for anesthesiology.7  Since then, it has been used for a variety of neurological, ophthalmological, gastroenterological, cardiological, and physiotherapeutic purposes, as well as for intensive care and resuscitation.

Galantamine crosses the blood-brain barrier freely8 and has not been found to accumulate in tissue.9  Side effects are rare, especially compared with drugs used for Alzheimer's disease, such as tacrine.

Although there is little evidence for the continuous use of galantamine as a restorative of lost or declining cognitive functions in European systems of folk medicine, other phytonutrients do have a long history, such as Melissa officinalis, Salvia elegans, and Artemisia absinthium.10 These have also been known to activate nicotinic receptors. Nevertheless, studies of galantamine in clinical usage indicate that it is one of the most extraordinary of these phytonutrients in terms of its scope.  Studies have shown it to be valuable for psychogenic impotence, or psychologically caused sexual dysfunction.  One study found that 30 days of treatment with 10 mg of galantamine taken three times daily resulted in stabilizing erectile function and eliminating premature ejaculation in 108 of 170 men, a 64% success rate.11

Galantamine - Gift from the Gods
The modern rediscovery of galantamine alluded to in the accompanying article led eventually to a startling hypothesis regarding the Odyssey, Homer's epic celebration of heroic memory. Our current knowledge of pharmacology and ethnobotany suggests that the "drug" delivered by Hermes, the messenger of the gods, to Odysseus to enable him to rescue his crew of sailors from the mind-numbing spell that the sorceress Circe had put them under was probably galantamine! The spell, in Homer's description, bore the earmarks of atropine (from jimsonweed).

Atropine is an anticholinergic, a substance that disrupts the brain's acetylcholine-mediated messaging system, resulting in cognitive dysfunction and memory impairment. The ideal antidote to such a drug would be an acetylcholinesterase inhibitor, and Homer's description of Hermes' gift from the gods points to galantamine, which was well suited to the purpose.

How uplifting it is to think that Homer's imperishable words could convey to us, over the millennia since he composed them, the hidden messages that have allowed modern scientists to deduce some of the pharmacological knowledge of the ancients. Looking back on them, we think, "They still had so much to learn." But then, so do we.

* These benefits of nicotine are no where near enough to compensate for the harm it causes from smoking.  Nicotine is a deadly poison.

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  1. Greenblatt HM, Kryger G, Lewis T, Silman I, Sussman JL. Structure of acetylcholinesterase complexed with (-)-galanthamine at 3- resolution. FEBS Lett 1999 Dec 17;463(3):321-6.
  2. Callahan LM, Chow N, Cheetham JE, Cox C, Coleman PD. Analysis of message expression in single neurons of Alzheimer's disease brain. Neurobiol Aging 1998 Jan-Feb;19(1 Suppl):S99-105.
  3. Beeri R, Andres C, Lev-Lehman E, Timberg R, Huberman T, Shani M, Soreq H. Transgenic expression of human acetylcholinesterase induces progressive cognitive deterioration in mice. Curr Biol 1995 Sep 1;5(9):1063-71.
  4. Galantamine improves memory and learning ability in Alzheimer's patients. July 20, 1998.
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  7. Paskov DS, Stoyanov KA, Saev SK, Tenev KA, Mincheva ML. Clinical experience with Nivalin as anticholinesterase drug in anaesthesiological practice. Proc First Eur Congr Anesthesiol, Vienna, Sep 3-9, 1962.
  8. Cozanitis DA. Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of scopolamine (Hyoscine). Anaesthesist 1977 Dec;26(12):649-50.
  9. Thomsen T, Kewitz H. Selective inhibition of human acetylcholinesterase by galanthamine in vitro and in vivo. Life Sci 1990;46(21):1553-8.
  10. Wake G, Court J, Pickering A, Lewis R, Wilkins R, Perry E. CNS acetylcholine receptor activity in European medicinal plants traditionally used to improve failing memory. J Ethnopharmacol 2000 Feb;69(2):105-14.
  11. Ludianskii EA. On the use of anticholinesterase agents in the treatment of neurological diseases. Sov Med 1964 Mar;27:84-7.

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