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Hi Everyone: This,piece is 85 lines long but should clarify the NADH v. CoQ issue and give you some medical insight and references as well. Hope it helps. I am a Ph.D. biochemical geneticist who also has remained silent too long as the discussion of NADH and CoQ goes on here. I work with these compounds and related substances daily as my major professional interest is in the diagnosis of metabolic muscle disease. CoQ or ubiquinone is NOT the same thing as NADH (just as others have mentioned in earlier notes here). They do work together, however, in moving electrons down a "handshake" system of complexes (5 in all) called the respiratory chain located in the mitochondria of every nucleated cell in the body. NADH does its work at the front end of this chain reaction and CoQ is located right in the middle of the chain. You may ask,"What is the point of passing electrons down a chain of complexes in the mitochondrion anyway?" Well, the point is to generate energy called ATP for the body's use; and by the way, oxygen is required to make it happen. So I think of mitochondria as the "lungs" of the cell. That is, mitochondria need to take in oxygen in order to fuel the process of making energy for the body thru electron transport. Those electrons I mentioned are derived originally from substances that are broken down (metabolized) by enzyme systems.. the substances are pretty big, like proteins, fats, and sugars. The electrons that are generated thru this digestive process are picked up by NAD (nicotinamide adenine dinucleotide) reducing the NAD to NADH (the first "handshake"). NADH then dumps the electrons at the beginning of the respiratory chain at a place called Complex I, the second handshake ( this complex is just that, "complex"; it contains enzymes named NADH dehydrogenase and NADH cytochrome c reductase, and NADH CoQ reductase), the electrons continue to get passed down the chain to enzymes in other complexes(II thru IV). In a way, the electrons kind of "pick up speed" as they pass down thru the chain all for the end result of making energy or ATP. Meanwhile, CoQ also carries electrons into the chain at about the middle (complex III) of it. There's also a substance called FAD that carries electrons into the chain at complex II. If anything goes wrong anywhere in the chain of events (like not enough fats or proteins supplied or transported to generate the electrons, or inadequate NAD to pick up electrons, or inadequate CoQ to pick up electrons, or mutations in any of the component subunits of the complexes preventing them from receiving electrons) then there will be a disruption in the production of ATP in the long run. Now what does all this have to do with the brain, PD, etc.? Well, that's under investigation as we speak. First, we know which tissues rely most on oxygen as a necessity for survival and they are the brain first, heart and skeletal muscle next, liver, and so on. So if there is any disruption in the respiratory chain or any of its parts, the brain may experience the ill effects first. There have been studies of PD patients in which deficiencies in complex I, in particular, have been found in their blood platelets and in there substantia nigra (autopsy studies). These deficiencies have been only partial, never 100% or even close, but they have been statistically significant when the studies have been done carefully (age-matched,etc.). (You see they MUST be age-matched studies because EVERYONE'S respiratory chain goes to pot with time...maybe that's a little strong, everyone's respiratory chain function "diminishes" as they age). The deficiencies are not found in all PD patients so no one knows quite what to make of it all. (I think we all know by now that PD is a "collection of disorders" that may have multiple causes and ages of onset.) Some of the other complexes have also been reported to be defective in some patients. But this must be kept in perspective. Profound defects in the respiratory chain are the hallmarks of other neuromuscular diseases called "mitochondrial myopathies" or "mitochondrial encephalomyopathies" when seizures and other neurologic symptoms are present in addition to muscle disease. In these disorders, the enzymes I mentioned above are often much more severely affected than what has been observed in "some" PD patients. So we must ask "are the respiratory chain defects found in PD patients secondary to their primary problems or causative?" ...no one knows for sure. In the meantime, some people may try CoQ therapy to "stoke up" their respiratory chain function but the fact is you don't even know if your particular respiratory chain needs that boost. I have never heard of using NADH as a therapy for anything and I haven't been able to find anything on it in the medical literature so I can't comment on its use or efficacy (that's not to say it hasn't been tested as a therapy because I know some of you have mentioned some sort of studies but have they been controlled trials?). I could tell you about the outcomes of some cases of mitochondrial myopathies which have been treated with cofactors such as CoQ, vitamin C, riboflavin, and vitamin K3, but these are topics for another discussion if anyone is interested. They may have no bearing in the long run on PD. Believe me, as a caregiver for PD patients in my family for over 30 yrs, I wish as much as any of you that the mitochondrial connection may have some significance in PD esp. since mitochondrial medicine is my professional interest, but I personally think it's secondary to a bigger problem. One thing to watch for in the medical news is the damage inflicted by free radicals on the mitochondrial DNA (which contains genes that code for some of the proteins in the complexes I described above). This I DO believe in because we all pick up more and more free radical damage with age. It may be that PD patients are even more susceptible so keep up with your anti-oxidants (vits. E, C, A). There is evidence that with age, our mitochondrial DNA gets increasingly damaged and that this damage is even greater in certain areas of the brain in PD patients and in patients with other neurodegenerative disorders such as Alzheimer's disease. In a recent review I read on CoQ (Ernster L and Dallner G.Biochemical, physiological and medical aspect of ubiquinone function, Biochimica Biophysica Acta 1995;1271:195-204), the authors state that ubiquinone not only serves as a coenzyme in electron transport in the respiratory chain but in its reduced form (ubiquinol) it also serves as an antioxidant. Also, by the way, since CoQ is synthesized by all tissues de novo, it technically does not qualify as a vitamin. As a dietary supplement, CoQ may enhance the protection of low density lipoproteins from oxidation and prevent free radical damage caused by neutrophils in inflammatory disease. In another reference I have, a layman's book on aging (Stop Aging Now! by Jean Carper, Harper Collins Publ. 1995), the chapter on CoQ discusses its use in treating patients with congestive heart failure. You may want to look at this book as it has chapters on all the vitamins and minerals important in aging and antioxidant therapy. Well, for those of you who like brief news summaries here, this was not one of them and I apologize for running on but I thought I might be able to clarify the NADH v. CoQ thing and bring in a few medical points that connect. Hope it helps. Send me your comments and questions and I'll do my best to answer or to find answers for you in the literature. Wishing the best for you all, Delana Vaughan