This is a reprint of my latest post on NADH - It might be helpful to any new
inquiries on NADH.
Lisa Carper
 
 
>
>(When all else fails, start typing :) ; sorry for all my confusing posts)
>Once again, following is an excerpt from an article on Coenzyme Q10 (ten),
NADH and Parkinson's. I realize the article (excerpt) from The Life
Extension Magazine is not scientific proof however, the study they are
talking about is from Harvard Med School, Mass General Hospital. I spoke
with Mass General and they are supposed to fax the actual study soon. For
those who may not know, my husband Jeff (PD 6yrs, 45) has taken NADH (4 x
2.5/day) along with a number of vitamins, herbs and so on. Since starting
this regemin we have noticed a considerable improvement in his energy level
and PD symptons. How much of his improved condition is the NADH, a
particular vitamin, herb or any combination will (we) will can't prove,
however we are confident in our judgement of Jeff's improved condition.
Please make comments freely.
>My Very Best Holiday Wishes For All of You, Lisa Carper
>
>CoQ and Nicotinamide Protect AGainst Neurotoxicity
>
>MPTP is a neurotoxin that produces clinical, biochemical, and
neuropathologic changes in both animals and humans, which are analogous to
those found in Parkinson's Disease. Doctors discovered that MPTP could
induce Parkinsonism when young people using it as a street drug began to
exhibit the symptons of Parkinson's Disease.
>Since Parkinson's Disease is characterized by the deterioration of
dopamine-producing cells and the excessive degradation of dopamine by the
enzyme monoamine oxidase B (MAO-B), the life extension drug deprenyl, which
is a selective MAO-B inhibitor and antioxidant can effectively counter the
neurotoxic effects of MPTP.
>Now there is a new study from the Neurochemistry Laboratory at Harvard
Medical School showing that CoQ and/or nicotinamide can counter the effects
of mild and moderate MPTP neurotoxicity, and that the combination of both
compounds is more effective than either one alone.
>
>NADH-The High Energy Compound
>(an excerpt for article on Coenzyme Q10, The Life Extension Magazine, Feb '96
>
>Nicotinamide, in its reduced form NADH, is a high energy compound which is
essential for energy production within cells, and which also stimulates the
biosynthesis of dopamine, the neurotransmitter which is depleted in
Parkinson's Disease. In the June 1995 issue of Life Extension Magazine, we
reported that NADH has been used effectively by Dr. Georg Birkmayer of the
University of Graz in Vienna to treat patients with Parkinson's Disease,
Alzheimers' Disease, and depression.
>This new study provides further support for the use of NADH for the
treatment of Parkinson's Disease and suggests that the combination of CoQ10
and NADH could be an effective treatment for this disease. It also lends
support to the hypothesis that the decline in energy production with
advancing age plays a critical role in the genesis and expression of all the
diseases of aging.
>
>ABSTRACT
>(This abstract and the actual study are available directly from Mass
General Hospital/Harvard Medical School)
>
>Coenzyme Q10 and nicotinamide and a free radical spin trap protect against
MPTP neurotoxicity.
>
>Schulz JB; Henshaw DR; Matthews RT; Beal MF
>Neurochemistry Laboratory, Massachusetts General Hospital, Boston 02114, USA
>Exp Neurol (United States) Apr 1995,132 (2) p279-83
>
>1-Methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) produces Parkinsonism
in both experimental animals and in man. MPTP is metabolized to
1-methyl-4-phenylpridinium, an inhibitor of mitochondrial comple I. MPTP
administration produces ATP depletions in vivo, which may lead to secondary
excitotoxicity and free radical generation. If this is the case then agents
which improve mitochondrial function or free radical scavengers should
attenuate MPTP neurotoxicity. In the present experiments three regimens of
MPTP administration produced varying degrees of striatal dopamine depletion.
A combination of coenzyme Q10 and nicotinamide protected against both mild
and moderate depletion of dopamine. In the MPTP regimen which regemin which
produced mild dopamine depletion nicotinamide or the free radical spin trap
N-tert-butyl-alpha-(2-sulfonphenyl)-nitrone were also effective. There was
no protection with a MPTP regimen which produced severe dopamine depletion.
These results show that agents which improve mitochondrial energy production
(coenzyme Q10 and nicotinamide NADH) and free radical scavengers can
attenuate mild to moderate MPTP neurotoxicity.
>
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