(Dimethyl Amino Ethanol Bitartrate)
DMAE is a supplement reported to minimize buildup of lipofuscin (age spots) in the brain. It plays a participatory role in acetycholine synthesis. DMAE has been shown to stimulate vivid, lucid dreams, suggesting possible sleep pattern enhancement. It is also used in anti-aging and memory enhancement.
Published Clinical Studies
[Therapeutic measures in tardive dyskinesia]1
Tegeler J, Woller W.
Studies on the treatments for neuroleptic-induced tardive dyskinesia published in the literature are reviewed. The great number of different treatments and the controversial results of most studies show that there is as yet no specific and safe treatment for tardive dyskinesia. Suggestions for well-designed treatment studies are given: Placebo-controlled double-blind design, larger patient populations, clear diagnostic and standard observing and rating conditions using different assessment methods and videotapes, withdrawal of neuroleptics and antiparkinsonian drugs to discover reversible tardive dyskinesia. If this procedure is not feasible, neuroleptics and other drugs should be maintained at a stable dose level. Longer term studies of some months are necessary to study the prolonged efficacy of different drugs. The effect of dopamine-antagonists such as neuroleptics and of dopamine-depleting agents such as reserpine and oxypertine is of limited duration. Dopamine-agonists such as L-Dopa, bromocriptine and amantadine help only few patients and may even aggravate the symptoms of tardive dyskinesia. In some double-blind studies cholinergic drugs such as lecithin and deanol have improved tardive dyskinesia, but further controlled studies are needed. Anticholinergic drugs such as antiparkinsonian agents should not be prescribed because they may aggravate tardive dyskinesia. Some patients respond to GABA-ergic agents such as baclofen, sodium valproate and the benzodiazepines, but further studies are needed before the value of GABA-ergic agents in the treatment of tardive dyskinesia can be properly assessed. After withdrawal of neuroleptics the average of remission rates within a year is 20%-30%. Elderly patients are more likely to have persistent dyskinesias. A progressive stepwise diminution of the neuroleptic dose and of the antiparkinsonian agents is recommended. When a patient's psychosis is exacerbated after withdrawal of the neuroleptics and tardive dyskinesia is also present, small doses of thioridazine, clozapine or tiapride can be administered. If this practice is not successful cholinergic or GABA-ergic agents may be useful. Because no currently available therapeutic agents satisfies the criteria of safety, marked effectiveness and prolonged efficacy in the treatment of tardive dyskinesia, prevention becomes more important. Prolonged use of a neuroleptic medication requires careful evaluation of indications and risks. The doses of neuroleptic drugs during the maintenance treatment of schizophrenia should be as small as possible.
PMID: 6136457 [PubMed - indexed for MEDLINE]
Ethanolamine analogues stimulate DNA synthesis by a mechanism not involving phosphatidylethanolamine synthesis.
Kiss Z, Crilly KS.
The Hormel Institute, University of Minnesota, Austin 55912, USA.
Dimethylethanolamine (0.5-1 mM), added to serum-starved NIH 3T3 fibroblasts, stimulated DNA synthesis 11-32-fold, and it also greatly enhanced the relatively modest (15-20-fold) mitogenic effect of insulin. Ethanolamine and monomethylethanolamine alone had no effects on DNA synthesis, but they also enhanced the stimulatory effect of insulin, although less effectively than dimethylethanolamine did. Lower concentrations (2.5-5 microg/ml) of compound D 609 (tricyclo-9-yl-xanthogenate), which had no effects on phospholipase activities, synergistically enhanced the combined effects of ethanolamine analogs and insulin on DNA synthesis without affecting the synthesis of ethanolamine phospholipids. These results suggest that ethanolamine and its analogues, formed by phospholipase D-mediated hydrolysis of ethanolamine phospholipids, may have growth regulatory functions independent of their role as phospholipid precursors.
PMID: 8641441 [PubMed - indexed for MEDLINE]
N-methyl bases of ethanolamine prevent apoptotic cell death induced by oxidative stress in cells of oligodendroglia origin.
Brand A, Gil S, Yavin E.
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
A major reason for brain tissue vulnerability to oxidative damage is the high content of polyunsaturated fatty acids (PUFAs). Oligodendroglia-like OLN 93 cells lack PUFAs and are relatively insensitive to oxidative stress. When grown in serum-free defined medium in the presence of 0.1 mM docosahexaenoic acid (DHA; 22:6 n-3) for 3 days, OLN 93 cells release in the medium 2.6-fold more thiobarbituric acid-reactive substances (TBARS) after a 30-min exposure to 0.1 mM H2O2 and 50 microM Fe2+. Release of TBARS was substantially decreased by approximately 20 and 30% on coincubation with either 1 mM N-monomethylethanolamine or N,N'-dimethylethanolamine (dEa), respectively. The protective effect of dEa was concentration- and time-dependent and was still visible after dEa removal, suggesting a long-lasting mechanism of protection. After 24 h following H2O2-induced stress, cell death monitored by cell sorting showed 16% of the cells in the sub-G1 area, indicative of apoptotic cell death. DHA-supplemented cultures showed 35% cell death, whereas cosupplements with dEa reduced cell death to 12%, indicating cell rescue. Although the exact mechanism for this protection is not known, the nature of the polar head group and the degree of unsaturation may determine the ultimate resistance of nerve cells to oxidative stress.
PMID: 10737617 [PubMed - indexed for MEDLINE]