Neuroprotective Effects of CoQ10 Supplementation:
A new study on endothelins reveals some
of the mechanisms through which Coenzyme Q10 may exert neuroprotective
effects. Endothelins are potent vasoconstrictors found in the body.
Ongoing research implicates them in a host of vascular disorders
contributing to hypertension, atherosclerosis, congestive heart failure
and kidney failure, and evidence is mounting of their involvement in
stroke. When endothelins are injected into the brains of animals, the
result is cellular energy decline, acidosis, excitotoxicity, depletion
of cellular antioxidants, and eventually the collapse of brain cell
metabolism. However, when Coenzyme Q10 was administered prior to
injection of the endothelins, it protected the antioxidant defenses of
brain cells and restored them to normal metabolic function. In
particular, Coenzyme Q10 exerted a marked sparing effect on the key
cellular antioxidants glutathione and superoxide dismutase (SOD), and
normalized cellular energy production (ATP) and lactate levels
(acidosis) in 24 hours.
Endothelins play a particularly important
role in cerebral vasospasm. About 2% of adults have aneurysms, a
balloon-like deformation in cerebral blood vessels. When an aneurysm
ruptures, the two out of three patients who survive the initial cerebral
hemorrhage face several possible complications. The most common serious
complication is “second stroke,” the cerebral vasospasm. This is a
prolonged narrowing of a blood vessel that causes ischemia in the
downstream brain tissue.
Researchers at the Polish Academy of
Sciences Medical Research Center tested the protective effect of
Coenzyme Q10 in a rabbit model of cerebral vasospasm. They blocked
arteries to reduce cerebral blood supply and later injected blood into
the brain to simulate hemorrhage. Following the injection, one group of
rabbits was given Coenzyme Q10 orally three times a day while the other
group was left untreated. All of the untreated rabbits displayed
significant neurological deficits (Grade 3 or 4) or died. None of the
rabbits given Coenzyme Q10 displayed a noticeable neurological deficit,
and all of them survived. Microscopic examination revealed no lesions in
the brain tissue of the Coenzyme Q10 treated group, whereas multiple
lesions “suggestive of degeneration or disappearance of neurons… and of
myelin disintegration” were found in brain tissue from the untreated
rabbits (Grieb P et al., 1997)1.
The underlying causes of cerebrovascular
disease suggest that Coenzyme Q10 may have a preventive effect. Most
cerebrovascular disease results from atherosclerosis or hypertension.
Atherosclerosis narrows blood vessels in the brain, making it easier for
blockages to develop; dislodged atherosclerotic plaque can itself cause
blockages. Hypertension is the most common cause of hemorrhagic stroke.
As discussed earlier in this series, Coenzyme Q10 helps protect against
the oxidative damage that leads to atherosclerosis, and may aid in
controlling blood pressure. Animal studies suggest that Coenzyme Q10
helps reverse age-related loss of arterial tone, which contributes to
both cerebrovascular and cardiovascular disease. And of course Coenzyme
Q10 plays a unique role in sustaining brain bioenergetics. While the
potential of Coenzyme Q10 in stroke prevention and treatment appears
promising, we can only hope that clinical trials will soon be undertaken
to test this propositon.
Stroke may mimic long-term genetic
effects of aging. Research in mice recently found that stroke causes
some of the same mitochondrial DNA deletions associated with aging. The
researchers speculate that there could be a single mechanism at work,
however much further research is needed before stroke research can be
meaningfully applied to brain aging.
See References
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