4.5 Article

Cerebral oxygen metabolism in patients with early Parkinson's disease

Journal

JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 313, Issue 1-2, Pages 123-128

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2011.09.010

Keywords

Parkinson's disease; Energy metabolism; CBF; CMRO2; Oxygen; Normalization; Positron emission tomography

Funding

  1. Danish National Science Foundation
  2. Medical Research Council of Denmark
  3. Lundbeck Foundation
  4. Danish Parkinson Foundation

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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 (CMRO2). To test this hypothesis, we compared CMRO2 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 CMRO2 and CBF. Between-group differences were evaluated for absolute data and intensity-normalized values. Results: No group differences were detected in regional magnitudes of CMRO2 or CBF. Upon normalization using the reference cluster method, significant relative CMRO2 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 CMRO2 in brain of PD patients, employing data-driven intensity normalization revealed widespread relative CMRO2 decreases in cerebral cortex. The detected pattern was very similar to that reported in earlier CBF and CMRgIc 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 CMRO2, CBF, and CMRgIc in spatially contiguous cortical regions in early PD, and support the hypothesis that ETC dysfunction could be a primary pathogenic mechanism in early PD. (C) 2011 Elsevier B.V. All rights reserved.

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