According to the following article
Comparing the youngest age people to the oldest, the number of striatal dopamine transporters was cut by 46%, or 6.6% per decade of life.3
The rate of loss of dopamine transporters is accelerated in Parkinson's patients, and this age-related factor may suggest why the disease progresses more rapidly in older patients. Some researchers are asking: Could a coenzyme Q10 deficiency be a starting point of this domino effect?
Will Parkinson's be cured in the near future?
Those suffering from Parkinson's have pinned their hopes on several potential therapies that might reverse the course of the disease. Stem cell therapy has received the most publicity because it offers the simple-to-understand approach of re-populating the brain with the very dopamine-producing cells that are destroyed by the disease. Findings from animal studies indicate that embryonic stem cells proliferate extensively and can generate dopamine-producing neurons suitable for possible cell replacement therapy for Parkinson's disease.4
How Coq10 Protects Brain Cells
Mitochondrial dysfunction is at the basis of many neurodegenerative diseases. The mitochondria are the "powerhouses" of cells, providing energy that fuel critical cellular functions. Aging and cumulative oxidative stress, however, impede the functioning of the mitochondria over time, resulting in dysfunction and demise.
Neuro-degenerative diseases involve early and accelerated nerve cell destruction. One of the primary causes of neuronal death is excitotoxicity, whereby the brain becomes over-sensitized to the neurotransmitter glutamate, whose role it is to send excitatory impulses.
Some scientists theorize that excitotoxicity can also result from a diminished energy level among neurons, which may lower their defenses against various neurotoxins and thus precipitate malfunctioning and death. Researchers now suggest that this bioenergy decline may be intimately involved with the progression of Parkinson's disease. Coenzyme Q10 seems to offer protection for neurons against the excitotoxicity of exposure to L-glutamate.*
The region of the brain affected by Parkinson's disease is also afflicted by excessive oxidative stress, more than is evident elsewhere in the brain. This oxidative stress is especially damaging to neurons whose energy levels are already taxed by neurotoxicity and excitotoxicity. According to a study published in a year 2001 issue of Neurotoxicology,* both neurotoxins and excitotoxins are "thought to involve free radical production, compromised mitochondrial activity and excessive lipid peroxidation." Logic would suggest then that restoring neuronal energy levels might boost these defenses and research has demonstrated that to be the case.
*Mazzio E et al. Effect of antioxidants on L-glutamate and N-methyl-4-phenylpyridinium ion induced-neurotoxicity in PC12 cells. Neurotoxicology 2001 Apr;22(2):283-8.
Another potential treatment involves the surgical insertion of electrodes into the brain to stimulate nerve impulses in a region called the subthalamic nucleus. This new therapy is called "Deep Brain Stimulation." A study published in a year 2002 issue of the journal Surgical Neurology showed significant improvement in all motor function tests in 36 advanced Parkinson's patients. These patients were able to reduce their use of the drug L-Dopa by an average of 53%, with daily "off-times" reduced by 35%! Dyskinesia, which is an impairment of voluntary muscle movement, also markedly improved after "Deep Brain Stimulation" therapy.5,6
It might also be possible to treat Parkinson's disease by altering the genes in brain cells responsible for causing motor abnormalities. A year 2002 article published in the journal Science showed that a gene transfer technique could protect dopamine producing neurons and rescue parkinsonian behavioral abnormalities in rats. The scientists who conducted this research indicated that this gene transfer technology could be used to induce therapeutic benefit.7
A clinical trial at the University of Kentucky is currently treating 10 Parkinson's patients with a bioengineered protein, called glial cell line-derived neurotrophic factor (GDNF), using a new drug-delivery method that sends the protein deep into the substantia nigra region of the brain where dopamine is produced. A constant supply of GDNF is administered by a pump implanted in the chest. So far, GDNF seems both to shield healthy brain cells from the disease and cause damaged cells to regenerate. According to University of Kentucky investigator Greg Gerhardt, after just a few months of testing, there is evidence of improvement in patients. In addition, British doctors reported in April 2002 that a similar trial in Bristol, England, improved muscle control of all five patients tested within a month of treatment.
These recent breakthroughs indicate a possible cure for Parkinson's disease in the foreseeable future. The question that Parkinson's patients ask today is: Can something be done to slow the progression of their disease? A growing number of researchers are looking at coenzyme Q10 as a potential treatment. Coenzyme Q10 acts as a critical energy carrier in mitochondrial electron transport. It also functions as an antioxidant to inhibit lipid peroxidation that kills dopamine producing neurons.8 According to a study published in a year 2002 issue of Neurochemistry Research, scientists believe that coenzyme Q10 works by improving cellular respiration, preventing oxidative stress, and inhibiting neuronal cell death.
To date, various investigators have found that coenzyme Q10 may be useful as a neuroprotective agent for diseases marked by mitochondrial dysfunction. This includes ALS (Lou Gehrig's disease), Huntington's chorea, Friedreich's ataxia and Parkinson's disease. Coenzyme Q10 is presently being studied as a potential treatment for early Parkinson's disease, as well as in combination with another drug as a potential treatment for Huntington's disease.9
A promising approach to slow Parkinson's progression
A new approach to Parkinson's disease was presented at the 2002 annual meeting of the American Neurological Association (New York City, Oct. 13-16) and simultaneously published in the journal Archives of Neurology. Dr. Clifford Shults and colleagues at the University of California, San Diego showed that oral coenzyme Q10 can actually slow the progression of Parkinson's disease.10
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While CoQ10 has been successfully tested in clinical trials for other neurological disorders including Huntington's Disease, this is the first human trial to test CoQ10 in a major neurodegenerative disease affecting millions of Americans. The multicenter study randomly assigned 80 people with early Parkinson's disease, who were not yet being treated, to either a placebo or coenzyme Q10 at dosages of 300, 600 or 1200 milligrams per day. All of the coenzyme Q10 dosages were safe and well-tolerated during the 16-month trial.
The patients in the study were assessed on the Unified Parkinson Disease Rating Scale (UPDRS) to establish baseline scores for their basic motor skills, mental status, mood and behavior, and ability to perform daily living activities. Since the scale is designed to measure disease progression, lower UPDRS scores indicate better performance. Results showed that the UPDRS score increased by 11.99 for the placebo group, 8.81 for the 300-milligrams/day group, 10.82 for the 600-milligrams/day group, and 6.69 for the 1200-milligrams/day group.
Basically, these findings demonstrate that coenzyme Q10 supplementation at 1200 milligrams/day resulted in 44% less mental and physical disability than a placebo. In addition, reported Shults, "the greatest benefit was seen in activities of daily living: dressing, bathing, eating and walking." The patients in the 1200 milligrams/day group were better able to function, and maintained greater independence for a longer time.
Several years ago, the same research team (Shults et al.) found that coenzyme Q10 levels were much lower (35%) in the mitochondria from parkinsonian patients than in age- and sex-matched controls, and that these lower concentrations seemed to relate to diminished activity of enzyme complexes vital for mitochondrial function.11 In that study, the authors concluded:
"The causes of Parkinson's disease are unknown, [but] evidence suggests that mitochondrial dysfunction and oxygen free radicals may be involved in its pathogenesis. The dual function of coenzyme Q10 as a constituent of the mitochondrial electron transport chain and a potent antioxidant suggest that it has the potential to slow the progression of Parkinson's disease."
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Should Parkinson's patients take CoQ10?
Confirmatory findings
Neurologist M. Flint Beal and colleagues at the Massachusetts General Hospital and Harvard Medical School has spent years proving that coenzyme Q10 has neuro-protective properties that may help diseases such as Parkinson's and Huntington's. Dr. Beal has a growing body of research to support his hypothesis.12 Earlier research had established that patients with early, untreated Parkinson's disease have reduced activities of the electron transport complexes I and II/III in mitochondria from platelets, which seems to be attributable to the Parkinson's disease process.13 For example, results indicated that complex II/III activity was reduced by 20% in Parkinson's disease compared with age-/sex-matched controls.
In a later study, oral supplementation with coenzyme Q10 in one-year old mice attenuated MPTP (1-methyl-4-phenyl-1,2,3,tetrahydropyridine) mediated neurotoxicity, which has been shown to cause a parkinsonian syndrome in test animals.14 The researchers put four groups of one-year-old male mice on either a standard diet or a diet supplemented with coenzyme Q10 for five weeks. At four weeks, one of the standard diet groups and one of the supplemented groups were treated with MPTP. Striatal dopamine concentrations and dopaminergic axon density were reduced in both MPTP-treated groups, but they were much higher, 37% and 62%, respectively, in the group first treated with coenzyme Q10 and then MPTP compared to the group treated with MPTP alone.
The unpleasant symptoms of Parkinson's disease
Classic Parkinson's symptoms are characterized by tremors or shaking of one or both arms and sometimes of other muscles. Generally muscles are weak and rigid, movements slow and the face expressionless, also the voice becomes weak. Typically the walk is with slow, short, shuffling steps, the arms held stiffly at the sides and the trunk slightly bent forward; the patient may spontaneously break into a shuffling run.
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Beal's team also demonstrated in middle-aged and old-aged rats, that coenzyme Q10 administration could restore levels of the nutrient to those of younger rats. The results showed that coenzyme Q10 levels rose by 10% to 40% in the mitochondria of the cerebral cortex region of the brain.14 What many people don't understand is that increasing serum or tissue levels of a nutrient through oral administration doesn't necessarily translate into some measurable disease-fighting or anti-aging benefit. That's what made this study's findings so promising. They showed that two months of supplementation resulted not only in replenished coenzyme Q10 levels in the brain and the brain mitochondria, but also in a significant increase of 29% in mitochondrial energy expenditure in the brain. Moreover, topping up coenzyme Q10 levels helped counter the neurodegenerative effects of an experimental neurotoxin administered to the dopamine-producing (striatal) region of the brain in the test rats.
The same study also showed that coenzyme Q10 might help other neurodegenerative diseases, such as Huntington's and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease). The researchers found that the administration of coenzyme Q10 could restore concentrations, prevent nerve-cell degeneration, and extend survival in transgenic mice bred with a familial form of ALS genes.
Meanwhile, a pilot study showed that energy production in the central nervous system and muscle of Huntington's disease patients is impaired. But two or more months of coenzyme Q10 supplementation at 360 milligrams per day resulted in significant improvements in biochemical markers of energy production in 83% of patients.
Additional research findings suggest that coenzyme Q10 supplementation may also help various forms of ataxia, particularly cases that show a decreased level of coenzyme Q10 in their muscles. For example, UK scientists at the University of Oxford found marked improvements in mitochondrial defects among Friedreich's ataxia (FA) patients, which involve a deficiency of a mitochondrial protein called frataxin. Six months of antioxidant treatment with coenzyme Q10 (400 milligrams/day) and vitamin E (2100 IU/day) in 10 Friedreich's Ataxia patients resulted in a 178% increase in the cardiac phosphocreatine to ATP ratio and 139% increase in the maximum rate of skeletal muscle mitochondrial ATP production. These results were observed after only three months of treatment, and were sustained after the six month study was completed.15
In another example, a study of six patients with hereditary ataxia revealed baseline coenzyme Q10 levels that were 70% below normal.16 However, following daily supplementation with coenzyme Q10, ranging from 300 milligrams to 3,000 milligrams, all of them had improved strength, ataxia and fewer seizures, and some were even able to walk. After a year of supplementation, patient scores on an ataxia symptom scale improved by an average of 25%.
Doctors remain cautious
Despite the hail of good news regarding the usefulness of coenzyme Q10 for Parkinson's and other neurodegenerative diseases, the mood among researchers is one of cautious optimism. For example, even Shults, lead author of the latest study, suggests that, before recommending coenzyme Q10 supplementation for Parkinson's disease patients, he would like to conduct a larger study, one that will more definitively determine coenzyme Q10's effects, especially in high doses. That upcoming study will likely involve about 400 patients taking doses of over 1200 milligrams per day for a longer study period.
Meanwhile, the National Institute of Neurological Disorders and Stroke, which helped fund the study, said that findings were "very promising," but called it premature to recommend coenzyme Q10 to Parkinson's patients until a larger trial is done. Scientists are also concerned about the purity of commercial CoQ10 supplements (i.e. how much coenzyme Q10 is actually in a product?), and what risks may exist as far as side effects, drug interactions and other contraindications. These scientists believe that more data is necessary in order to establish safe and effective doses of coenzyme Q10 for neurodegenerative diseases.
While the ideal or most effective dose cited in the latest study is 1200 milligrams daily, that's five times the upper dose consumed for prevention purposes. There is, however, strong historical data regarding the safety of congestive heart failure patients taking about 300 milligrams a day of coenzyme Q10 and those suffering from Huntington's disease using 600 mg/day.
Why Parkinson's patients can't wait
Parkinson's disease is a progressive degenerative brain disorder that is currently incurable. Patients suffer increasing debilitating complications as the disease progresses. Today's therapies only mitigate the agonizing symptoms-they do not slow the rate of deterioration.
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Even when treatments such as "Deep Brain Stimulation" become widely available, the benefits may only be partial. It is thus imperative for Parkinson's patients to protect as many dopamine-producing neurons as possible. The latest study indicates that high-dose coenzyme Q10 does just that.
For the first time in medical history, a human study has shown that the progression of Parkinson's disease can be slowed by 44% when patients consume 1200 mg of coenzyme Q10 a day.
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