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CoenzymeQ10-Coq10 Assists in Fighting Parkinson's Disease:
In Parkinson’s disease, cell death is
highly selective. Neurons that produce the neurotransmitter dopamine die
in a part of the brain that coordinates movement. This depletes dopamine
stores and leads to muscle rigidity, tremor and difficulty initiating
movement.
The specific brain region affected in
Parkinson’s disease, the substantia nigra, has the highest level of
mitochondrial DNA mutation in the brain. Evidence is mounting that
mitochondrial DNA mutations cause cellular respiration to malfunction in
Parkinson’s disease, exactly as Linnane’s theory would predict.
Parkinson’s disease patients show defective cellular respiration in the
first complex of the cellular respiratory chain.
Beal and colleagues found that the
bioenergetic deficit in Parkinson’s disease patients correlates strongly
with Coenzyme Q10 levels. In follow-up research, they tested Coenzyme
Q10 on mice treated with a neurotoxin (MPTP) whose effects mimic
Parkinson’s disease. The toxin caused significantly less damage to the
dopamine system in the brains of mice that had been fed Coenzyme Q10 for
the previous five weeks.
Beal’s group also tested the bioenergetic
effect of oral Coenzyme Q10 supplements in Parkinson’s disease patients.
They found that Coenzyme Q10 restored the depressed activity of the
first complex of the cellular respiratory chain to approximately normal
levels, and was most effective at 600 mg per day. The scientists
emphasized, however, that a larger study is required to determine
whether the trend toward significance of these results will be
validated. Furthermore, a new study shows that oral Coenzyme Q10 also
increases the activity of the second complex of the cellular respiratory
chain in the brains of normal mice.
Scientists hypothesize that the
bioenergetic defect in Parkinson’s disease “lowers the threshold” for
programmed cell death. Energetically deficient neurons are less able to
tolerate oxidative stress, which then triggers the cellular “decision to
die.” Oxidative stress is particularly high even under normal conditions
in the region of the brain affected by Parkinson’s disease, which may
help explain why additional oxidative stress depresses cells in that
particular region beyond the threshold for programmed cell death.
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