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From the Turku PET Centre (N.M.K., S.A., K.N., S.H., A.B., V.O., J.O.R.) and Department of Pharmacology and Clinical Research Services Turku (CRST) (M.K., M.S.), University of Turku, Department of Psychology (S.A.), óbo Akademi University, Turku City Hospital (M.V.), Department of Clinical Radiology, Turku University Hospital (R.P.), Turku Imanet Ltd (J.O.R.), Turku, Finland; GE Healthcare Medical Diagnostics (I.A.W.), UK; and Clinical Geriatrics (M.V.), Karolinska Institutet, Stockholm, Sweden.
Address correspondence and reprint requests to Dr Rinne, Turku PET Centre, University of Turku, P.O. Box 52, FIN-20521 Turku, Finland; e-mail: juha.rinne{at}tyks.fi
Background: PET studies with N-methyl-[11C]2-(4':-methylaminophenyl)-6-hydroxybenzothiazole ([11C]PIB) have revealed an increased tracer uptake in several brain regions in Alzheimer disease (AD).
Objective: To employ voxel-based analysis method to identify brain regions with significant increases in [11C]PIB uptake in AD vs healthy control subjects, indicative of increased amyloid accumulation in these regions.
Methods: We studied 17 patients with AD and 11 control subjects with PET using [11C]PIB as tracer. Parametric images were computed by calculating a region-to-cerebellum ratio over 60 to 90 minutes in each voxel. Group differences in [11C]PIB uptake were analyzed with statistical parametric mapping (SPM) and automated region-of-interest (ROI) analysis.
Results: SPM showed increased uptake (p < 0.001) in the frontal, parietal, and lateral temporal cortices as well as in the posterior cingulate and the striatum. No significant differences in uptake were found in the primary sensory and motor cortices, primary visual cortex, thalamus, and medial temporal lobe. These results were supported by automated ROI analysis, with most prominent increases in AD subjects in the frontal cortex ([11C]PIB uptake 163% of the control mean) and posterior cingulate (146%) followed by the parietal (146%) and temporal (145%) cortices and striatum (133%), as well as small increases in the occipital cortex (117%) and thalamus (115%).
Conclusions: Voxel-based analysis revealed widespread distribution of increased [11C]PIB uptake in Alzheimer disease (AD). These findings are in accordance with the distribution and phases of amyloid pathology in AD, previously documented in postmortem studies.
This article was previously published in electronic format as an Expedited E-Pub on September 13, 2006, at www.neurology.org
Supported by EVO grants from Turku University Hospital and by grants from the Finnish Medical Society Duodecim, the Finnish Cultural Foundation, the Research Foundation of Orion Corporation, the Päivikki and Sakari Sohlberg Foundation, the Sigrid Juselius Foundation, and the Research Council for Health of the Academy of Finland (project no. 205954).
Disclosure: J.O.R. has a consultancy agreement with Turku Imanet, a subsidiary of GE Healthcare. M.K. and M.S. are employees of CRST, a contract research unit of the University of Turku, with contract research support from Imanet/GE administered by the University.
Received December 22, 2005. Accepted in final form June 15, 2006.
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