DMAE

Summary (The Good, The Bad, and all other Essential Benefits/Effects/Facts Information)

DMAE is a compound that is known as a mind health compound. It does this by reducing buildup of what is known as the 'age pigment', which impairs cognitive function and is implicated in the cognitive decline with age. It can also increase levels of the compound involved with memory, acetylcholine.

It can also protect neurons and other cells from harmful effects of certain types of oxidation by embedding itself in the structure of the cell and acting as an anti-oxidant, as well as sustaining metabolic processes in the body through a process known as 'methyl donation'.

DMAE is also found in various face and body creams, and can tighten and tone skin quality.

Also Known As

Dimethylaminoethanol, dimethylethanolamine, Deanol (cream)

Do Not Confuse With

DMAA

Is a Form of

• Cholinergic

Goes Well With

• Racetams

Things to Note

Via increasing acetylcholine levels, DMAE is slightly stimulatory.

Caution Notice (just some FYI - if needed)

DMAE may potentially be teratogenic (causing defects in unborn infants) in the first few days after impregnation and should not be used orally by women who are attempting to conceive.

Detailed Summary

1. Effects in the Brain
2. Treatment of Tardive Dyskinesia
3. Cosmetic Potential
4. DMAE as a Teratogenic Substance

Edit1. Effects in the Brain

Many studies done use the compound Centrophenoxine, which exerts many of its benefits vicariously through DMAE, of which is a subset thereof. For these reasons many studies that are conducted on centrophenoxine usually also apply to DMAE.

DMAE is able to reduce build-up of beta-amyloid pigmentation, a pigment 'waste-product' that is associated and possibly casuative of neurological decline with age and Alzheimer's.^[1] This trait of DMAE is shared with other lipid-permeable acetylcholine analogues such as serotonin and vanillylamine. It is also highly efficacious in reducing levels of lipofuscin, a specific beta-amyloid pigment found in neurons and glial cells.^[2]

DMAE can act in a longevity-enhancing fashion via being incorporated into cell membranes as phosphatidyl-DMAE. As a structural anti-oxidant of cell membranes, Phosphatidyl-DMAE can scavenge OH- ions which would normally lead to membrane damage and thus alleviate damage to the membrane over time. This mechanism of action is the same as the compound Centrophenoxine.^[3] This scavenging of OH- free radicals may also be the reason behind DMAEs protective effects against protein cross-linking in the brain^[4] and may be through either direct anti-oxidation or competition with OH- ions with proline and hydroxyproline, of which the latter can bind with OH- to form nitroxyl radicals whereas DMAEs binding to OH- ions is non-oxidative.^[5] By the same mechanism, DMAE can also protect against Iron overload toxicity in neurons.

Edit2. Treatment of Tardive Dyskinesia

DMAE supplementation has been shown in some studies to show an small albeit nonsignificant positive trend for symptoms in Tardive Dyskinesia^[6], but typically it is seen as an ineffective treatment.^[7][8]

Edit3. Cosmetic Potential

DMAE, in the form of facial cream, is being looked at for improving skin quality for aging skin when applied as a 3% facial cream.^[9] It shows benefits in improving the appearance of coarse wrinkles, under-eye dark circles, nasolabial folds, sagging neck skin, and neck firmness and is generally very well tolerated.

Most notably, DMAE as a facial gel increases skin firmness.^[10][11]

Edit4. DMAE as a Teratogenic Substance

Although preliminary, it seems that DMAE may aggravate or induce the formation of neural tube defects, as evidenced by in vitro studies on mouse embryonic cells.^[12] Under normal conditions, rat embryos uptake choline and convert it into phosphatidylcholine(PC) as an active substrate. DMAE supplementation seems to replace choline usage when it is present due to higher affinity and competition but fails to convert into PC due to an apparent lack of expression of the enzyme phosphatidylethanolamine methyltransferase (PeMT) in embryos. This enzyme is absolutely necessary for the conversion of Phosphatidylethanolamine into PC.^[13]

Essentially, DMAE competitively inhibits Choline uptake during the first few days of neural tube formation (1-10 days after impregnation), but the embryo is not yet able to use DMAE as well as an adult due to an immature CDP-choline metabolic pathway and underexpression of key enzymes.

These mechanisms should not occur in adult cells due to the activity of the PeMT enzyme and a mature CDP-choline metabolic enzyme pathway.

Scientific Support & Reference Citations

References

1. Buznikov GA, et al. Sea urchin embryonic development provides a model for evaluating therapies against beta-amyloid toxicity. Brain Res Bull. (2008)
2. Sharma D, Maurya AK, Singh R. Age-related decline in multiple unit action potentials of CA3 region of rat hippocampus: correlation with lipid peroxidation and lipofuscin concentration and the effect of centrophenoxine. Neurobiol Aging. (1993)
3. Zs-Nagy I. On the role of intracellular physicochemistry in quantitative gene expression during aging and the effect of centrophenoxine. A review. Arch Gerontol Geriatr. (1989)
4. Nagy I, Nagy K. On the role of cross-linking of cellular proteins in aging. Mech Ageing Dev. (1980)
5. Nagy I, Floyd RA. Electron spin resonance spectroscopic demonstration of the hydroxyl free radical scavenger properties of dimethylaminoethanol in spin trapping experiments confirming the molecular basis for the biological effects of centrophenoxine. Arch Gerontol Geriatr. (1984)
6. Tammenmaa IA, et al. Systematic review of cholinergic drugs for neuroleptic-induced tardive dyskinesia: a meta-analysis of randomized controlled trials. Prog Neuropsychopharmacol Biol Psychiatry. (2004)
7. Jeste DV, Wyatt RJ. Therapeutic strategies against tardive dyskinesia. Two decades of experience. Arch Gen Psychiatry. (1982)
8. Soares KV, McGrath JJ. The treatment of tardive dyskinesia--a systematic review and meta-analysis. Schizophr Res. (1999)
9. Grossman R. The role of dimethylaminoethanol in cosmetic dermatology. Am J Clin Dermatol. (2005)
10. Uhoda I, et al. Split face study on the cutaneous tensile effect of 2-dimethylaminoethanol (deanol) gel. Skin Res Technol. (2002)
11. Tadini KA, Campos PM. In vivo skin effects of a dimethylaminoethanol (DMAE) based formulation. Pharmazie. (2009)
12. Fisher MC, et al. Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro. FASEB J. (2002)
13. Hirata F, et al. Identification and properties of two methyltransferases in conversion of phosphatidylethanolamine to phosphatidylcholine. Proc Natl Acad Sci U S A. (1978)

Last Updated: Aug 3, 2011 15:38:32