Co Q10 Therapy for Parkinson Disease

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http://archneur.ama-assn.org/issues/current/ffull/ned20014.html

 

 

Mitochondrial Therapy for Parkinson Disease

 

 

Roger N. Rosenberg, MD

 

 

 

THE PRECISE causes of Parkinson disease (PD) are beginning to be defined and

include specific genetic mutations causal of autosomal dominant (alpha-synuclein

mutations) and recessive (Parkin mutations) phenotypes and for sporadic PD, an

interaction between genetic and environmental factors.1, 2 An important emerging

molecular defect is impaired function of the mitochondrial electron transport

chain, particularly inhibition of complexes I and II/III, leading to failure of

adenosine triphosphate synthesis. Inhibition of complex I by MPTP

(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) can cause human parkinsonism.3, 4

Schapira and colleagues5 have found a selective decrease in complex I activity

in postmortem PD substantia nigra but not in patients with multiple system

atrophy. Untreated PD patients have reduced activity of complexes I and II/III

in mitochondria isolated from platelets.6 Shults et al7 have demonstrated

reduced levels of coenzyme Q10 in the mitochondria from platelets isolated from

PD patients. Beal et al8 have shown that oral supplementation with coenzyme Q10

reduced the loss of dopamine and dopaminergic axons in the striatum in

1-year-old mice treated with MPTP.

 

In this issue of the ARCHIVES, Shults and colleagues9 with the Parkinson Study

Group have studied the effects of coenzyme Q10 in patients with early PD.

Patients were selected who were not treated with any medication for PD or with

any antioxidants such as selegiline or vitamin E or C within 60 days of the

baseline period. Eighty PD patients were entered into the study and randomly

assigned to placebo or coenzyme Q10 at 300, 600, or 1200 mg/d. Patients were

evaluated with the Unified Parkinson Disease Rating Scale (UPDRS) at baseline

and at months 1, 4, 8, 12, and 16 and were followed up until the patient was

treated with levodopa or for a maximum of 16 months. Of great interest, they

found a reduction in the decline of the total UPDRS, with the greatest reduction

in the decline being in the activity of daily living subscores. The reduction in

the worsening of the UPDRS was observed in all 3 dosages of coenzyme Q10;

however, the greatest effect was in the highest dosage of 1200 mg/d.

 

Their data are supportive of the view that mitochondrial dysfunction does play a

role in the pathogenesis of sporadic PD and that further research using coenzyme

Q10 at higher dosages should be studied. It will be important to define whether

the defects of mitochondrial complexes I and II/III are acquired genetic

mutations and whether they are due to environmental toxins or primary congenital

mutations, inherited maternally, which cause a genetic predisposition for PD.

Clearly, the data of the Parkinson Study Group in this article are intriguing

and provocative therapeutic findings and offer considerable potential hope for

future allied therapies.

 

 

 

Author/Article Information

 

 

Roger N. Rosenberg, MD

Editor

University of Texas Southwestern Medical Center

5323 Harry Hines Blvd

Dallas, TX 75390-9108

 

 

 

 

 

REFERENCES

 

 

1.

Vaughan JR, Davis MB, Wood NW.

Genetics of Parkinson's disease.

Ann Hum Genet.

2001;65(pt 2):111-126.

MEDLINE

 

 

2.

Sherer TB, Betarbet R, Greenamyre JT.

Pathogenesis of Parkinson's disease.

Curr Opin Investig Drugs.

2001;2:657-662.

MEDLINE

 

 

3.

Langston JW, Ballard P, Tetrud JW, Irwin I.

Chronic parkinsonism in humans due to a produce of meperidine-analog synthesis.

Science.

1983;219:979-980.

MEDLINE

 

 

4.

Prezedborski S, Jackson-Lewis V.

Mechanisms of MPTP toxicity.

Mov Disord.

1998;13(suppl 1):35-38.

 

 

 

5.

Schapira AHV, Mann VM, Cooper JM, et al.

Anatomic disease specificity of NADH CoQ1 reductase complex I deficiency in

Parkinson's disease.

J Neurochem.

1990;55:2142-2145.

MEDLINE

 

 

6.

Haas R, Nasirian F, Nakano K, et al.

Low platelet mitochondrial complex I and complex II/III activity in early

untreated Parkinson's disease.

Ann Neurol.

1995;37:714-722.

MEDLINE

 

 

7.

Shults CW, Haas RH, Passov D, Beal MF.

Coenzyme Q10 levels correlate with the activities of complexes I and II/III in

mitochondria from parkinsonian and nonparkinsonian subjects.

Ann Neurol.

1997;42:261-264.

MEDLINE

 

 

8.

Beal MF, Matthews RT, Tieleman A, Shults CW.

Coenzyme Q10 attenuates the 1-methyl-4-phenyl-1,2,3,6, tetrahydropyridine (MPTP)

induced loss of striatal dopamine and dopaminergic axons in aged mice.

Brain Res.

1998;783:109-114.

MEDLINE

 

 

9.

Shults CW, Oakes D, Kieburtz K, et al, and the Parkinson Study Group.

Effects of coenzyme Q10 in early Parkinson disease: evidence for slowing of the

functional decline.

Arch Neurol.

2002;59:1541-1550.

ABSTRACT | FULL TEXT | PDF | MEDLINE

 

 

 

 

 

 

 

 

 

 

 

 

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