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