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Life Extension Magazine

LE Magazine February 2003

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Should Parkinson's patients take CoQ10?

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Parkinson's disease is the second most common degenerative brain disorder. The percentage of the population afflicted by Parkinson's is on the rise.1

The symptoms of Parkinson's disease are attributed to a loss of cells in the substantia nigra region of the brain. These cells produce dopamine, a critical neurotransmitter responsible for motion control. As Parkinson's disease progressives, an accelerated rate of cell death occurs, resulting in even less dopamine being produced and the manifestation of more pronounced complications.

Today's treatments only address symptoms. These therapies don't protect against the underlying pathologies implicated in Parkinson's disease, namely the death of dopamine-producing neurons (brain cells). Drugs such as L-Dopa provide dopamine to the brain and temporarily alleviate symptoms. These drugs, however, do not slow the progression of the disease. At advanced stages, the drugs fail to work and complications become severe.

Researchers question why some people develop Parkinson's while others escape its clutches. One of the answers under consideration is that low coenzyme Q10 concentrations may predispose certain individuals to the disease. Coenzyme Q10 is naturally synthesized by the body and is a crucial component of the cell's energy cycle. As people age, they produce far less coenzyme Q10, which helps explain the heightened risk of Parkinson's with advancing age.2

In a year 2002 study, Yale scientists examined a group of healthy people ranging in age from 18 to 88 using a neuro-imaging technique. The researchers observed a steady decline in "striatal dopamine transporters," a marker of brain degeneration characteristic of Parkinson's disease. 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."

Continued on Page 2 of 2

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