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Mitochondrial Therapy for Parkinson Disease
Arch Neurol. 2002;59:1523.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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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
. . . [Full Text of this Article]
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