DMAE

DMAE is a Choline molecule with one less methyl group, and has the ability to reduce build-up of the age pigmentation known as beta-amyloid. It is the active component of Centrophenoxine, or Lucidril, a pharmaceutical designed for cognitive health in the elderly.

This page features 11 unique references to scientific papers.


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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.

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Also Known As

Dimethylaminoethanol, dimethylethanolamine, Deanol (cream)


Do Not Confuse With

DMAA (Stimulant), DHEA (Hormone Precursor)


Things to Note

Via increasing acetylcholine levels, DMAE is slightly stimulatory.

Is a Form of


Goes Well With


Stacks Part Of increased usefulness


    Caution Notice

    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.

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    Table of Contents:


    Edit1. Neurology

    1.1. Rheology

    DMAE (0.6% in vitro) appears to protect from iron-induced oxidation and subsequent protein cross-linking, thought to preserve membrane fluidity via anti-oxidative effects,[1] either directly or by preventing formation of Nitroxyl radicals (hydroxyl radical binding with hydroxyproline) by non-oxidatively sequestering hydroxyl radicals.[2]

    1.2. Alzheimer's Disease

    V0191 (DMAE Pyroglutamate) in 55-90 year old persons (mean age 72.2) with mild cognitive impairment taking 1500mg of the supplement daily at breakfast over 24 weeks noted that although there was a trend to more response with treatment than placebo (defined as more than a 4 point improvement on the ADAS-cog rating scale), there were no statistically significant improvements nor improvement on global assessments.[3]

    1.3. Tardive Dyskinesia

    DMAE supplementation has been shown in some studies to show an small albeit nonsignificant positive trend for symptoms in Tardive Dyskinesia[4], but typically it is seen as an ineffective treatment.[5][6]


    Edit2. Interactions with Aesthetics

    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.[7] 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.[8][9]


    Edit3. Safety and Toxicity

    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.[10] 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.[11]

    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.

    References

    1. Nagy I, Nagy K. On the role of cross-linking of cellular proteins in aging. Mech Ageing Dev. (1980)
    2. 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)
    3. Dubois B, et al. Effect of six months of treatment with V0191 in patients with suspected prodromal Alzheimer's disease. J Alzheimers Dis. (2012)
    4. 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)
    5. Jeste DV, Wyatt RJ. Therapeutic strategies against tardive dyskinesia. Two decades of experience. Arch Gen Psychiatry. (1982)
    6. Soares KV, McGrath JJ. The treatment of tardive dyskinesia--a systematic review and meta-analysis. Schizophr Res. (1999)
    7. Grossman R. The role of dimethylaminoethanol in cosmetic dermatology. Am J Clin Dermatol. (2005)
    8. Uhoda I, et al. Split face study on the cutaneous tensile effect of 2-dimethylaminoethanol (deanol) gel. Skin Res Technol. (2002)
    9. Tadini KA, Campos PM. In vivo skin effects of a dimethylaminoethanol (DMAE) based formulation. Pharmazie. (2009)
    10. Fisher MC, et al. Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro. FASEB J. (2002)
    11. Hirata F, et al. Identification and properties of two methyltransferases in conversion of phosphatidylethanolamine to phosphatidylcholine. Proc Natl Acad Sci U S A. (1978)

    (Common misspellings for DMAE include DMEA, DAME)

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