Cerebral oxygen metabolism in patients with early Parkinson's disease

Per Borghammer, Paul Cumming, Karen Østergaard, Albert Gjedde, Anders Rodell, Christopher J Bailey, Manoucher S Vafaee

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Abstrakt

AIM: Decreased activity of the mitochondrial electron transport chain (ETC) has been implicated in the pathogenesis of Parkinson's disease (PD). This model would most likely predict a decrease in the rate of cerebral oxygen consumption (CMRO(2)). To test this hypothesis, we compared CMRO(2) and cerebral blood flow (CBF) PET scans from PD patients and healthy controls.

MATERIALS AND METHODS: Nine early-stage PD patients and 15 healthy age-matched controls underwent PET scans for quantitative mapping of CMRO(2) and CBF. Between-group differences were evaluated for absolute data and intensity-normalized values.

RESULTS: No group differences were detected in regional magnitudes of CMRO(2) or CBF. Upon normalization using the reference cluster method, significant relative CMRO(2) decreases were evident in widespread prefrontal, parieto-occipital, and lateral temporal regions. Sensory-motor and subcortical regions, brainstem, and the cerebellum were spared. A similar pattern was evident in normalized CBF data, as described previously.

CONCLUSION: While the data did not reveal substantially altered absolute CMRO(2) in brain of PD patients, employing data-driven intensity normalization revealed widespread relative CMRO(2) decreases in cerebral cortex. The detected pattern was very similar to that reported in earlier CBF and CMRglc studies of PD, and in the CBF images from the same subjects. Thus, the present results are consistent with the occurrence of parallel declines in CMRO(2), CBF, and CMRglc in spatially contiguous cortical regions in early PD, and support the hypothesis that ETC dysfunction could be a primary pathogenic mechanism in early PD.

OriginalsprogEngelsk
TidsskriftJournal of the Neurological Sciences
Vol/bind313
Udgave nummer1-2
Sider (fra-til)123-8
Antal sider6
ISSN0022-510X
DOI
StatusUdgivet - 15. feb. 2012

Bibliografisk note

Copyright © 2011 Elsevier B.V. All rights reserved.

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