Parkinson's Disease: New Coenzyme Q10 Research


Results of the first placebo-controlled, multicenter clinical trial of the
compound coenzyme Q10 suggest that it can slow disease progression in
patients with early-stage Parkinson's disease (PD). While the results must
be confirmed in a larger study, they provide hope that this compound may
ultimately provide a new way of treating PD.

The phase II study, led by Clifford Shults, M.D., of the University of
California, San Diego (UCSD) School of Medicine, looked at a total of 80 PD
patients at 10 centers across the country to determine if coenzyme Q10 is
safe and if it can slow the rate of functional decline. The study was funded
by the National Institute of Neurological Disorders and Stroke (NINDS) and
appears in the October 15, 2002, issue of the 'Archives of Neurology'. (1)

"This trial suggested that coenzyme Q10 can slow the rate of deterioration
in Parkinson's disease," says Dr. Shults. "However, before the compound is
used widely, the results need to be confirmed in a larger group of
patients."

PD is a chronic, progressive neurological disease that affects about 500,000
people in the United States.  It results from the loss of brain cells that
produce the neurotransmitter dopamine and causes tremor, stiffness of the
limbs and trunk, impaired balance and coordination, and slowing of
movements. Patients also sometimes develop other symptoms, including
difficulty swallowing, disturbed sleep, and emotional problems.  PD usually
affects people over the age of 50, but it can affect younger people as well.
While levodopa and other drugs can ease the symptoms of PD, none of the
current treatments has been shown to slow the course of the disease.

The investigators believe coenzyme Q10 works by improving the function of
mitochondria, the "powerhouses" that produce energy in cells. Coenzyme Q10
is an important link in the chain of chemical reactions that produces this
energy. It also is a potent antioxidant -- a chemical that "mops up"
potentially harmful chemicals generated during normal metabolism.  Previous
studies carried out by Dr. Shults, Richard Haas, M.D., of UCSD and Flint
Beal, M.D., of Cornell University have shown that coenzyme Q10 levels in
mitochondria from PD patients are reduced and that mitochondrial function in
these patients is impaired.
Animal studies have shown that coenzyme Q10 can protect the area of the
brain that is damaged in PD.  Dr. Shults and colleagues also conducted a
pilot study with PD patients which showed that consumption of up to 800
mg/day of coenzyme Q10 was well-tolerated and significantly increased the
level of coenzyme Q10 in the blood.

All of the patients who took part in the new study had the three primary
features of PD -- tremor, stiffness, and slowed movements -- and had been
diagnosed with the disease within 5 years of the time they were enrolled.
After an initial screening and baseline blood tests, the patients were
randomly divided into four groups. Three of the groups received coenzyme Q10
at three different doses (300 mg/day, 600 mg/day, and 1,200 mg/day), along
with vitamin E, while a fourth group received a matching placebo that
contained vitamin E alone. Each participant received a clinical evaluation 1
month later and every 4 months for a total of 16 months or until the
investigator determined that the patient needed treatment with levodopa.
None of the participants or the study investigators knew which treatment
each patient had received until the study ended.
The investigators found that most side effects of coenzyme Q10 were mild,
and none of the patients required a reduction of their dose. The percentage
of people receiving coenzyme Q10 who reported side effects was not
significantly different from that of the placebo group. During the study
period, the group that received the largest dose of coenzyme Q10 (1,200
mg/day) had 44 percent less decline in mental function, motor (movement)
function, and ability to carry out activities of daily living, such as
feeding or dressing themselves. The greatest effect was on activities of
daily living. The groups that received
300 mg/day and 600 mg/day developed slightly less disability than the
placebo group, but the effects were less than those in the group that
received the highest dosage of coenzyme Q10. The groups that received
coenzyme Q10 also had significant increases in the level of coenzyme Q10 in
their blood and a significant increase in energy-producing reactions within
their mitochondria.

The results of this study suggest that doses of coenzyme Q10 as high as
1,200 mg/day are safe and may be more effective than lower doses, says Dr.
Shults. The findings are consistent with those of a recently published study
of patients with early Huntington's disease -- another degenerative
neurological disorder -- that showed slightly less functional decline in
groups that received 600 mg/day of coenzyme Q10.

Dr. Shults and his colleagues strongly caution patients against taking
coenzyme Q10 until a larger, definitive trial can be conducted. Because
coenzyme Q10 is classified as a dietary supplement, it is not regulated by
the U.S. Food and Drug Administration. The versions of the supplement sold
in stores may differ, they may not contain potentially beneficial amounts of
the compound, and taking coenzyme Q10 over a number of years may be costly,
says Dr. Shults. In addition, the current study included only a
small number of patients, and the findings may not extend to people in later
stages of PD or to those who  are at risk but have not been diagnosed with
the disorder, he notes. Finally, if many people begin taking coenzyme Q10
because of these early results, it might make it impossible for
investigators to find enough patients to carry out definitive studies of the
compound's effectiveness and the proper dosages, since patients must not be
taking any treatments in order to be considered for enrollment in a
definitive trial.

The investigators are now planning a larger clinical trial that will examine
the effects of 1,200 mg/day of coenzyme Q10, and possibly a higher dose as
well, in a larger number of patients.
Source: National Institute of Neurological Disorders and Stroke (NINDS)
The NINDS is a component of the National Institutes of Health in Bethesda,
Maryland, and is the nation's primary supporter of biomedical research on
the brain and nervous system.

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