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First published online January 21, 2009, 10.2967/jnumed.108.056499
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Journal of Nuclear Medicine Vol. 50 No. 2 191-197
© 2009 by Society of Nuclear Medicine

doi: 10.2967/jnumed.108.056499

Clinical Investigation

Detection of Alzheimer Pathology In Vivo Using Both 11C-PIB and 18F-FDDNP PET

Nelleke Tolboom1,2, Maqsood Yaqub1, Wiesje M. van der Flier2, Ronald Boellaard1, Gert Luurtsema1, Albert D. Windhorst1, Frederik Barkhof3, Philip Scheltens2, Adriaan A. Lammertsma1 and Bart N.M. van Berckel1

1 Department of Nuclear Medicine and PET Research, VU University Medical Centre, Amsterdam, The Netherlands; 2 Department of Neurology and Alzheimer Centre, VU University Medical Centre, Amsterdam, The Netherlands; and 3 Department of Radiology, VU University Medical Centre, Amsterdam, The Netherlands

Correspondence: For correspondence or reprints contact: Nelleke Tolboom, Department of Neurology and Alzheimer Centre, VU University Medical Centre, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands. E-mail: n.tolboom{at}vumc.nl

11C-Pittsburgh Compound-B (11C-PIB) and 18F-(2-(1-{6-[(2-[18F]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene) (18F-FDDNP) have been developed as PET tracers for in vivo imaging of pathology in Alzheimer's disease (AD). The purpose of this study was to directly compare these tracers in patients with AD, patients with mild cognitive impairment (MCI), and healthy controls. Methods: Paired 11C-PIB and 18F-FDDNP scans were acquired in 14 patients with AD, 11 patients with amnestic MCI, and 13 controls. For both tracers, parametric images of binding potential (BPND) were generated. Global cortical BPND was assessed using ANOVA. In addition, regional patterns of BPND were compared between diagnostic groups using ANOVA for repeated measures. Results: Global cortical BPND of 11C-PIB showed higher binding in patients with AD than in controls and patients with MCI. 18F-FDDNP uptake was higher in patients with AD than in controls, but MCI could not be distinguished from AD or from controls. Global BPND values of both tracers were moderately correlated (r = 0.45; P = 0.005). In MCI, BPND of 11C-PIB showed a bimodal distribution, whereas values for 18F-FDDNP were more widespread, with more MCI patients demonstrating increased uptake. Regional 11C-PIB binding showed different patterns across diagnostic groups, as AD patients showed an overall increase in binding, with the lowest binding in the medial temporal lobe. With 18F-FDDNP, patterns were similar across diagnostic groups. For all groups, highest values were observed in the medial temporal lobe. Conclusion: Differences in BPND between patients with AD, patients with MCI, and controls were more pronounced for 11C-PIB. The difference in regional binding, the moderate correlation, and the discrepant findings in MCI suggest that they measure related, but different, characteristics of the disease.

Key Words: 11C-PIB • Pittsburgh Compound-B • 18F-FDDNP • positron emission tomography • PET • amyloid • Alzheimer disease

COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.


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