Difference between revisions of "DMAE"

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[[Information on nutritional supplements people with ALS have been taking]]
  
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DMAE (2-dimethylaminoethanol) is a chemical that has been used to treat a number of conditions affecting the brain and central nervous system. Like other such treatments, it is thought to work by increasing production of the neurotransmitter acetylcholine, although this has not been proven. [1]
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[https://en.wikipedia.org/wiki/Dimethylethanolamine Wikipedia page]
  
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Because DMAE was believed to be a cholinergic, it has been tried for several neurological disorders. However, well-designed double-blind, placebo-controlled studies have yielded almost entirely negative results. 3-9 In addition, there is some controversy over whether DMAE really increases acetylcholine at all. [1]
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DMAE (2-dimethylaminoethanol) is a chemical that has been used to treat a number of conditions affecting the brain and central nervous system. Like other such treatments, it is thought to work by increasing production of the neurotransmitter acetylcholine, although this has not been proven. [a]
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DMAE is a free radical scavenger. {{#pmid:22300295|malanga2012}}
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Because DMAE was believed to be a cholinergic, it has been tried for several neurological disorders. However, well-designed double-blind, placebo-controlled studies have yielded almost entirely negative results. 3-9 In addition, there is some controversy over whether DMAE really increases acetylcholine at all. [a]
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Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors. {{#pmid:7264671|haubrich1981}}
  
 
== References ==
 
== References ==
  
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[1]
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[a] http://www.bidmc.org/YourHealth/Conditions-AZ/Amyotrophic-Lateral-Sclerosis.aspx?ChunkID=21390  
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http://www.bidmc.org/YourHealth/Conditions-AZ/Amyotrophic-Lateral-Sclerosis.aspx?ChunkID=21390  
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[2]
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[[Category:Supplement data pages]]
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<bibtex>
 
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@article{Manfredi2005,
 
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abstract = {Mitochondria play a pivotal role in many metabolic and apoptotic pathways that regulate the life and death of cells. Accumulating evidence suggests that mitochondrial dysfunction is involved in the pathogenesis of amyotrophic lateral sclerosis (ALS). Mitochondrial dysfunction may cause motor neuron death by predisposing them to calcium-mediated excitotoxicity, by increasing generation of reactive oxygen species, and by initiating the intrinsic apoptotic pathway. Morphological and biochemical mitochondrial abnormalities have been described in sporadic human ALS cases, but the implications of these findings in terminally ill individuals or in post-mortem tissues are difficult to decipher. However, remarkable mitochondrial abnormalities have also been identified in transgenic mouse models of familial ALS expressing mutant Cu, Zn superoxide dismutase (SOD1). Detailed studies in these mouse models indicate that mitochondrial abnormalities begin prior to the clinical and pathological onset of the disease, suggesting that mitochondrial dysfunction may be causally involved in the pathogenesis of ALS. Although the mechanisms whereby mutant SOD1 damages mitochondria remain to be fully understood, the finding that a portion of mutant SOD1 is localized in mitochondria, where it forms aberrant aggregates and protein interactions, has opened a number of avenues of investigation. The future challenges are to devise models to better understand the effects of mutant SOD1 in mitochondria and the relative contribution of mitochondrial dysfunction to the pathogenesis of ALS, as well as to identify therapeutic approaches that target mitochondrial dysfunction and its consequences.},
 
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author = {Manfredi, Giovanni and Xu, Zuoshang},
 
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doi = {10.1016/j.mito.2005.01.002},
 
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file = {:C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Manfredi, Xu - 2005 - Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.pdf:pdf},
 
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issn = {1567-7249},
 
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journal = {Mitochondrion},
 
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keywords = {Amyotrophic Lateral Sclerosis,Amyotrophic Lateral Sclerosis: etiology,Amyotrophic Lateral Sclerosis: genetics,Amyotrophic Lateral Sclerosis: pathology,Amyotrophic Lateral Sclerosis: physiopathology,Animals,Apoptosis,Disease Models, Animal,Mice,Mice, Transgenic,Mitochondria,Mitochondria: physiology,Models, Neurological,Motor Neurons,Motor Neurons: pathology,Motor Neurons: physiology,Mutation,Nerve Degeneration,Nerve Degeneration: pathology,Nerve Degeneration: physiopathology,Superoxide Dismutase,Superoxide Dismutase: genetics},
 
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month = apr,
 
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number = {2},
 
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pages = {77--87},
 
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pmid = {16050975},
 
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title = {{Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.}},
 
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url = {http://www.sciencedirect.com/science/article/pii/S1567724905000346},
 
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volume = {5},
 
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year = {2005}
 
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}
 
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</bibtex>
 

Latest revision as of 11:21, 12 January 2018

Information on nutritional supplements people with ALS have been taking

Wikipedia page

DMAE (2-dimethylaminoethanol) is a chemical that has been used to treat a number of conditions affecting the brain and central nervous system. Like other such treatments, it is thought to work by increasing production of the neurotransmitter acetylcholine, although this has not been proven. [a]

DMAE is a free radical scavenger. [1]

Because DMAE was believed to be a cholinergic, it has been tried for several neurological disorders. However, well-designed double-blind, placebo-controlled studies have yielded almost entirely negative results. 3-9 In addition, there is some controversy over whether DMAE really increases acetylcholine at all. [a]

Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors. [2]

References[edit]

[a] http://www.bidmc.org/YourHealth/Conditions-AZ/Amyotrophic-Lateral-Sclerosis.aspx?ChunkID=21390
  1. ↑ Malanga et al.: New insights on dimethylaminoethanol (DMAE) features as a free radical scavenger. Drug Metab Lett 2012;6:54-9. PMID: 22300295. Recently, a number of synthetic drugs used in a variety of therapeutic indications have been reported to have antiaging effects. Among them, Dimethylaminoethanol (DMAE), an anologue of dietylaminoethanol, is a precursor of choline, which in turn allows the brain to optimize the production of acetylcholine that is a primary neurotransmitter involved in learning and memory. The data presented here includes new information on the ability of the compound to scavenge specific free radicals, assessed by Electron Spectroscopic Resonance (EPR), to further analyze the role of DMAE as an antioxidant. DMAE ability to directly react with hydroxyl, ascorbyl and lipid radicals was tested employing in vitro assays, and related to the supplemented dose of the compound.
  2. ↑ Haubrich et al.: Deanol affects choline metabolism in peripheral tissues of mice. J. Neurochem. 1981;37:476-82. PMID: 7264671. Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors.
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