Difference between revisions of "DMAE"

Latest revision as of 11:21, 12 January 2018

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DMAE (2-dimethylaminoethanol) is a chemical that has been used to treat a number of conditions affecting the brain and central nervous system. Like other such treatments, it is thought to work by increasing production of the neurotransmitter acetylcholine, although this has not been proven. [a]

DMAE is a free radical scavenger. ^[1]

Because DMAE was believed to be a cholinergic, it has been tried for several neurological disorders. However, well-designed double-blind, placebo-controlled studies have yielded almost entirely negative results. 3-9 In addition, there is some controversy over whether DMAE really increases acetylcholine at all. [a]

Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors. ^[2]

References[edit]

1. ↑ Malanga et al.: New insights on dimethylaminoethanol (DMAE) features as a free radical scavenger. Drug Metab Lett 2012;6:54-9. PMID: 22300295. Recently, a number of synthetic drugs used in a variety of therapeutic indications have been reported to have antiaging effects. Among them, Dimethylaminoethanol (DMAE), an anologue of dietylaminoethanol, is a precursor of choline, which in turn allows the brain to optimize the production of acetylcholine that is a primary neurotransmitter involved in learning and memory. The data presented here includes new information on the ability of the compound to scavenge specific free radicals, assessed by Electron Spectroscopic Resonance (EPR), to further analyze the role of DMAE as an antioxidant. DMAE ability to directly react with hydroxyl, ascorbyl and lipid radicals was tested employing in vitro assays, and related to the supplemented dose of the compound.
2. ↑ Haubrich et al.: Deanol affects choline metabolism in peripheral tissues of mice. J. Neurochem. 1981;37:476-82. PMID: 7264671. Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors.