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Check out http:expasy.hcuge.ch/cgi-bin/show_image?P9&left76 All I know is it is a mutation of the flavoprotein fragment of NADH I don't know what N1,N2,N3,N4 are, have to look that up. NADH effects glutathione reductase, glutathione, anything that depends on glutathione, like alpha lipoic acid and dihydrolipoic acid that chelates metals, and glutathione protects the brain from lipid peroxidation.PD has too much lipid peroxidation. Alpha lipoic acid and dihydrolipoic acid are responsible for decarboxylation of dopa to dopamine and depend on glutathione. They are also responsible for making vitamin E and vitamin C. Adenylate cyclase is glutathione dependent, it is effected by pertussis that causes PD symptoms. NADH efffects thioredoxin which thiolates glutamate reductase and peroxide reductase. Stimulate glutamate receptors and you get PD, there is too much lipid peroxidation in PD. Thats why when you give isoleucine that transports fatty acids into the cells there is a decrease in tremors noted. NADH is part of complex I, NADH-ubiquitin oxioreductase that is low in PD. This effects G-proteins, diacyglycerol, arachadonic acid, fatty acids, adult onset diabetes, which is also effected by the IgE immune beta T-cells that come around to destroy the lewy bodies and screw up the insulin receptors causing insulin resistance. NADH-Complex I mutation would cause problems with protein kinase C that activates B vitamins. So many symptoms are the same as someone lacking B6. NADH effects A2Red that effects P450 or CYP2D6. It is low in PD. This is responsible for handling toxic environmental assaults, herbicides that cause PD. It is also responsible for the breakdown of at least 60 per cent of all the drugs a person takes, many of which cause PD symptoms. I would really like to know exactly what the defect is so maybe we can think of a way to fix it. I already know of glutathione reductase being made by plasmodium falciparum, don't know if a drug company is producing it. I know that if you had more of this you would have more dihydrolipoic acid to break down metals, protect the brain more from lipid peroxidation, be able to make more dopamine from dopa. NIFS is a B6 enzyme that breaks metal-sulfur bonds. Maybe this would break apart lewy bodies, stop the immune cells from killing what they think are foreign bodies, but are really brain cells. I've written to several scientists. None write back . It took me a year to figure out is was a problem in the falvoprotein fragment of NADH, last night I find a picture of it. Would love to find an article or two describing it. Thanks. [log in to unmask]