DMAE
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]
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]
References
[1] http://www.bidmc.org/YourHealth/Conditions-AZ/Amyotrophic-Lateral-Sclerosis.aspx?ChunkID=21390
[2] <bibtex> @article{Manfredi2005, 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.}, author = {Manfredi, Giovanni and Xu, Zuoshang}, doi = {10.1016/j.mito.2005.01.002}, 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}, issn = {1567-7249}, journal = {Mitochondrion}, 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}, month = apr, number = {2}, pages = {77--87}, pmid = {16050975}, title = Template:Mitochondrial dysfunction and its role in motor neuron degeneration in ALS., url = {http://www.sciencedirect.com/science/article/pii/S1567724905000346}, volume = {5}, year = {2005} } </bibtex>
