Hi Skibumm,
I found the original article on which that Prevention article was
based. The authors of the original have not published further
findings (the original was published in the fall of 2002, and picked
up by Prevention in spring 2003). However, several other researchers
have published scientific papers about Coenzyme Q10 and its effects on
Parkinson's disease since that one. I've pasted in the abstracts
below for you to read. If you'd like to get the full articles you'll
need to go through your local academic/medical library or get them via
interlibrary loan from your public library (I can't put in full text
of articles because of copyright law).
I found these articles in the PubMed database (www.pubmed.gov) using
the search "Co-Q10 AND parkinsons":
1: JAMA. 2004 Jan 21;291(3):358-64.
Neuroprotection in Parkinson disease: mysteries, myths, and misconceptions.
Schapira AH, Olanow CW.
Parkinson disease is an age-related neurodegenerative disease that affects
approximately 1 million persons in the United States. Current therapies provide
effective control of symptoms, particularly in the early stages of the disease,
but most patients develop motor complications with long-term treatment, and
features develop such as postural instability, falling, and dementia that are
not adequately controlled with existing medications. Accordingly,
neuroprotective therapy that might slow, stop, or reverse disease progression is
urgently needed. While many agents appear to be promising based on laboratory
studies, selecting clinical end points for clinical trials that are not
confounded by symptomatic effects of the study intervention has been difficult.
More recently, neuroimaging end points have been used as biomarkers of disease
progression, but again there are concerns that they may be influenced by
regulatory effects of the drugs used. We review clinical trials aimed at
detecting neuroprotection in Parkinson disease and address the controversies
surrounding the interpretation of these studies.
2: Ann N Y Acad Sci. 2003 Jun;991:120-31.
Mitochondria, oxidative damage, and inflammation in Parkinson's disease.
Beal MF.
The pathogenesis of Parkinson's disease (PD) remains obscure, but there is
increasing evidence that impairment of mitochondrial function, oxidative damage,
and inflammation are contributing factors. The present paper reviews the
experimental and clinical evidence implicating these processes in PD. There is
substantial evidence that there is a deficiency of complex I activity of the
mitochondrial electron transport chain in PD. There is also evidence for
increased numbers of activated microglia in both PD postmortem tissue as well as
in animal models of PD. Impaired mitochondrial function and activated microglia
may both contribute to oxidative damage in PD. A number of therapies targeting
inflammation and mitochondrial dysfunction are efficacious in the MPTP model of
PD. Of these, coenzyme Q(10) appears to be particularly promising based on the
results of a recent phase 2 clinical trial in which it significantly slowed the
progression of PD.
3: Neurosci Lett. 2003 May 8;341(3):201-4.
Coenzyme Q10 supplementation provides mild symptomatic benefit in patients with
Parkinson's disease.
Muller T, Buttner T, Gholipour AF, Kuhn W.
Features of Parkinson's disease (PD) include oxidative stress, nigral
mitochondrial complex I deficiency and visual dysfunction, all of which are also
associated with coenzyme Q(10) (CoQ(10)) deficiency. The objective of this
monocenter, parallel group, placebo controlled, double-blind trial was to
determine the symptomatic response of daily oral application of 360 mg CoQ(10)
lasting 4 weeks on scored PD symptoms and visual function, measured with the
Farnsworth-Munsell 100 Hue test (FMT), in 28 treated and stable PD patients.
CoQ(10) supplementation provided a significant (P=0.01) mild symptomatic benefit
on PD symptoms and a significantly (F((1,24))=8.48, P=0.008) better improvement
of FMT performance compared with placebo. Our results indicate a moderate
beneficial effect of oral CoQ(10) supplementation in PD patients.
4: Ann Neurol. 2003;53 Suppl 3:S39-47; discussion S47-8.
Bioenergetic approaches for neuroprotection in Parkinson's disease.
Beal MF.
There is considerable evidence suggesting that mitochondrial dysfunction and
oxidative damage may play a role in the pathogenesis of Parkinson's disease
(PD). This possibility has been strengthened by recent studies in animal models,
which have shown that a selective inhibitor of complex I of the electron
transport gene can produce an animal model that closely mimics both the
biochemical and histopathological findings of PD. Several agents are available
that can modulate cellular energy metabolism and that may exert antioxidative
effects. There is substantial evidence that mitochondria are a major source of
free radicals within the cell. These appear to be produced at both the
iron-sulfur clusters of complex I as well as the ubiquinone site. Agents that
have shown to be beneficial in animal models of PD include creatine, coenzyme
Q(10), Ginkgo biloba, nicotinamide, and acetyl-L-carnitine. Creatine has been
shown to be effective in several animal models of neurodegenerative diseases and
currently is being evaluated in early stage trials in PD. Similarly, coenzyme
Q(10) is also effective in animal models and has shown promising effects both in
clinical trials of PD as well as in clinical trials in Huntington's disease and
Friedreich's ataxia. Many other agents show good human tolerability. These
agents therefore are promising candidates for further study as neuroprotective
agents in PD.
Even though they don't follow up your particular study, I hope you
find them interesting!
Librariankt |
Clarification of Answer by
librariankt-ga
on
07 Apr 2004 19:27 PDT
By the way, the original article was somewhat controversial, with a
comment in the issue of Archives of Neurology and two author
rebuttals. Here's the abstract and citation for the original:
Arch Neurol. 2002 Oct;59(10):1541-50.
Comment in:
Arch Neurol. 2002 Oct;59(10):1523.
Arch Neurol. 2003 Aug;60(8):1170-2; author reply 1172-3.
Arch Neurol. 2003 Aug;60(8):1170; author reply 1172-3.
Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the
functional decline.
Shults CW, Oakes D, Kieburtz K, Beal MF, Haas R, Plumb S, Juncos JL, Nutt J,
Shoulson I, Carter J, Kompoliti K, Perlmutter JS, Reich S, Stern M, Watts RL,
Kurlan R, Molho E, Harrison M, Lew M; Parkinson Study Group.
Department of Neurosciences, Mail Code 0662, University of California-San Diego,
9500 Gilman Dr, La Jolla, CA 92093-0662, USA. cshults@ucsd.edu
BACKGROUND: Parkinson disease (PD) is a degenerative neurological disorder for
which no treatment has been shown to slow the progression. OBJECTIVE: To
determine whether a range of dosages of coenzyme Q10 is safe and well tolerated
and could slow the functional decline in PD. DESIGN: Multicenter, randomized,
parallel-group, placebo-controlled, double-blind, dosage-ranging trial. SETTING:
Academic movement disorders clinics. PATIENTS: Eighty subjects with early PD who
did not require treatment for their disability. INTERVENTIONS: Random assignment
to placebo or coenzyme Q10 at dosages of 300, 600, or 1200 mg/d. MAIN OUTCOME
MEASURE: The subjects underwent evaluation with the Unified Parkinson Disease
Rating Scale (UPDRS) at the screening, baseline, and 1-, 4-, 8-, 12-, and
16-month visits. They were followed up for 16 months or until disability
requiring treatment with levodopa had developed. The primary response variable
was the change in the total score on the UPDRS from baseline to the last visit.
RESULTS: The adjusted mean total UPDRS changes were +11.99 for the placebo
group, +8.81 for the 300-mg/d group, +10.82 for the 600-mg/d group, and +6.69
for the 1200-mg/d group. The P value for the primary analysis, a test for a
linear trend between the dosage and the mean change in the total UPDRS score,
was.09, which met our prespecified criteria for a positive trend for the trial.
A prespecified, secondary analysis was the comparison of each treatment group
with the placebo group, and the difference between the 1200-mg/d and placebo
groups was significant (P =.04). CONCLUSIONS: Coenzyme Q10 was safe and well
tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects
assigned to coenzyme Q10 than in those assigned to placebo, and the benefit was
greatest in subjects receiving the highest dosage. Coenzyme Q10 appears to slow
the progressive deterioration of function in PD, but these results need to be
confirmed in a larger study.
-Librariankt
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