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Article type: Research Article
Authors: Kemppainen, Ninaa; b; * | Joutsa, Juhoa; c | Johansson, Jarkkoa | Scheinin, Noora M.a; d | Någren, Kjella; e | Rokka, Johannaa | Parkkola, Riittaf | Rinne, Juha O.a; b
Affiliations: [a] Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland | [b] Division of Clinical Neurosciences, Turku University Hospital and University of Turku, Turku, Finland | [c] Department of Clinical Neurophysiology, Turku University Hospital and University of Turku, Turku, Finland | [d] Department of Psychiatry, Turku University Hospital and University of Turku, Turku, Finland | [e] Department of Nuclear Medicine, PET and Cyclotron Unit, Odense University Hospital, Odense, Denmark | [f] Department of Radiology, Turku University Hospital and University of Turku, Turku, Finland
Correspondence: [*] Correspondence to: Nina Kemppainen, MD, PhD, Turku PET Centre, University of Turku, P.O. Box 52, FIN-20521 Turku, Finland. Tel.: +358 2 313 1866; Fax: +358 2 231 8191; nina.kemppainen@tyks.fi
Abstract: The aim of this longitudinal positron emission tomography (PET) study was to evaluate the interrelationship between brain metabolism and amyloid accumulation during the disease process from mild cognitive impairment (MCI) to Alzheimer’s disease (AD). Nine MCI patients, who converted to AD between two and five years, and nine healthy subjects underwent [11C]PIB and [18F]FDG PET scans at baseline and at 5 years. [11C]PIB uptake was clearly higher in MCI patients at baseline compared to controls and spread extensively to the cerebral cortex during the conversion to AD. [18F]FDG uptake was reduced especially in the temporal-parietal regions in MCI compared to controls at baseline, and widely over the cortex at the 5-year follow-up. The reduction in metabolism during the follow-up was significant in the posterior brain regions. In addition, brain amyloid load was positively associated with metabolism in posterior brain regions in MCI, but not after conversion to AD. The results suggest that there are interactions between brain amyloid accumulation and metabolism during the AD process, including a possible compensatory upregulation of posterior brain metabolism in the early phase.
Keywords: Alzheimer’s disease, [11C]PIB, [18F]FDG, follow-up, mild cognitive impairment, PET
DOI: 10.3233/JAD-150190
Journal: Journal of Alzheimer's Disease, vol. 48, no. 1, pp. 123-133, 2015
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