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Lookup NU author(s): Dr Michael FirbankORCiD, Professor Alison Yarnall, Dr Rachael LawsonORCiD, Dr Gordon Duncan, Dr Tien Kheng Khoo, Dr George Petrides, Professor John O'Brien, Dr Ross Maxwell, Professor David BrooksORCiD, Professor David BurnORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Objective To assess reductions of cerebral glucose metabolism in Parkinson’s disease (PD) with 18F-fluorodeoxyglucose (FDG) PET, and their associations with cognitive decline. Methods FDG-PET was performed on a cohort of 79 patients with newly diagnosed PD (mean disease duration 8 months) and 20 unrelated controls. PD subjects were scanned whilst on their usual dopaminergic medication. Cognitive testing was performed at baseline, and after 18 months using the Cognitive Drug Research (CDR) and Cambridge Neuropsychological Test Automated Battery (CANTAB) computerized batteries, the Mini-Mental State Exam (MMSE), and the Montreal Cognitive Assessment (MoCA). We used statistical parametric mapping (SPM12) software to compare groups and investigate voxelwise correlations between FDG metabolism and cognitive score at baseline. Linear regression was used to evaluate how levels of cortical FDG metabolism were predictive of subsequent cognitive decline rated with the MMSE and MoCA. Results PD subjects showed reduced glucose metabolism in the occipital and inferior parietal lobes relative to controls. Low performance on memory based tasks was associated with reduced FDG metabolism in posterior parietal and temporal regions, whilst attentional performance was associated with more frontal deficits. Baseline parietal to cerebellum FDG metabolism ratios predicted MMSE (beta =0.38, p=0.001) and MoCA (beta=0.3, p=0.002) at 18 months controlling for baseline score. Conclusions Reductions in cortical FDG metabolism were present in newly diagnosed PD, and correlated with performance on neuropsychological tests. A reduced baseline parietal metabolism is associated with risk of cognitive decline and may represent a potential biomarker for this state and the development of PD dementia.
Author(s): Firbank MJ, Yarnall AJ, Lawson RA, Duncan GW, Khoo TK, Petrides GS, O'Brien JT, Barker RA, Maxwell RJ, Brooks DJ, Burn DJ
Publication type: Article
Publication status: Published
Journal: Journal of Neurology, Neurosurgery, and Psychiatry
Year: 2017
Volume: 88
Issue: 4
Pages: 310-316
Print publication date: 01/04/2017
Online publication date: 06/10/2016
Acceptance date: 19/08/2016
Date deposited: 23/08/2016
ISSN (print): 0022-3050
ISSN (electronic): 1468-330X
Publisher: BMJ Group
URL: http://dx.doi.org/10.1136/jnnp-2016-313918
DOI: 10.1136/jnnp-2016-313918
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