Editorial |

Mitochondrial Therapy for Parkinson Disease

Roger N. Rosenberg, MD
Arch Neurol. 2002;59(10):1523. doi:10.1001/archneur.59.10.1523.
Text Size: A A A
Published online


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.

Sign In to Access Full Content

Don't have Access?

Register and get free email Table of Contents alerts, saved searches, PowerPoint downloads, CME quizzes, and more

Subscribe for full-text access to content from 1998 forward and a host of useful features

Activate your current subscription (AMA members and current subscribers)

Purchase Online Access to this article for 24 hours

First Page Preview

View Large
First page PDF preview





Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Comment


Some tools below are only available to our subscribers or users with an online account.

Web of Science® Times Cited: 8

Sign In to Access Full Content

Related Content

Customize your page view by dragging & repositioning the boxes below.

See Also...
Articles Related By Topic
Related Topics
PubMed Articles

The Rational Clinical Examination
Make the Diagnosis: Parkinsonism

The Rational Clinical Examination
Original Article: Does This Patient Have Parkinson Disease?