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.
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.
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. 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.
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. 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.