Wednesday, August 14, 2013
Galantamine is by far my favorite nootropic. Not only is it a mild acetylcholinesterase inhibitor, it also positively modulates the alpha 7 nicotinine acetylcholine receptor. The end effect is a global increase in acetylcholine levels and the facilitation of the activation of the particular type of receptor intimately involved in learning and memory.
The strength of AchE inhibition is directly proportional to the reciprocal increase in the amount of acetylcholinesterase present. In other words, the stronger you inhibit the enzyme, the more the body produces to counteract its absence. This has been quantified in studies examining this effect with galantamine in comparison to donepezil, which saw much greater AchE enzyme elevation with donepezil. This isn't surprising since donepezil is roughly 40-300 times more potent at inhibiting this enzyme . In the context of Alzheimer's disease, or other forms of dementia, this fact is relatively unimportant since the user will continue to supplement with the AchE inhibitor until death. Conversely, for a healthy individual using an AchE inhibitor for a relatively shorter amount of time, this may result in fairly significant rebound once supplementation ceases. This effect would be considerably more muted when supplementing with galantamine, especially since nootropic effects can be seen with doses much smaller then what is required to inhibit AchE.