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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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Dimethylaminoethanol, dimethylethanolamine, Deanol (cream)
Via increasing acetylcholine levels, DMAE is slightly stimulatory.
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, either directly or by preventing formation of Nitroxyl radicals (hydroxyl radical binding with hydroxyproline) by non-oxidatively sequestering hydroxyl radicals.
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.
DMAE supplementation has been shown in some studies to show an small albeit nonsignificant positive trend for symptoms in Tardive Dyskinesia, but typically it is seen as an ineffective treatment.
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. 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.
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. 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.
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.
(Common misspellings for DMAE include DMEA, DAME)
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