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SAM-e: Difference between revisions
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==Pharmacology== | ==Pharmacology== | ||
Sam-e is an [[endogenous]] molecule that has numerous roles including methyl donation in neurotransmitter synthesis, antioxidative effects (radical scavenging, glutathione precursor), anti-inflammatory effects, and neuroprotective effects<ref>Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence. | http://www.ncbi.nlm.nih.gov/pubmed/12420702/</ref> | Sam-e is an [[endogenous]] molecule that has numerous roles including methyl donation in neurotransmitter synthesis, antioxidative effects (radical scavenging, glutathione precursor), anti-inflammatory effects, and neuroprotective effects.<ref>Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence. | http://www.ncbi.nlm.nih.gov/pubmed/12420702/</ref> | ||
Sam-e, in addition to providing ATP to the cell, also can convert Nicotinamine into N-methyl-nicotinamide (NMNA) via Nicotinamide N-methyltransferase, NMNA which can prevent choline efflux from the brain and neuron, a process which may account for some of Sam-e's [[nootropic]] effects.<ref>Nicotinamide homeostasis: a xenobiotic pathway that is key to development and degenerative diseases. | http://www.ncbi.nlm.nih.gov/pubmed/15922112</ref> | Sam-e, in addition to providing ATP to the cell, also can convert Nicotinamine into N-methyl-nicotinamide (NMNA) via Nicotinamide N-methyltransferase, NMNA which can prevent choline efflux from the brain and neuron, a process which may account for some of Sam-e's [[nootropic]] effects.<ref>Nicotinamide homeostasis: a xenobiotic pathway that is key to development and degenerative diseases. | http://www.ncbi.nlm.nih.gov/pubmed/15922112</ref> | ||