RT Journal Article
SR Electronic
T1 Comparison of Early-Phase <sup>11</sup>C-Deuterium-<span class="sc">l</span>-Deprenyl and <sup>11</sup>C-Pittsburgh Compound B PET for Assessing Brain Perfusion in Alzheimer Disease
JF Journal of Nuclear Medicine
JO J Nucl Med
FD Society of Nuclear Medicine
SP 1071
OP 1077
DO 10.2967/jnumed.115.168732
VO 57
IS 7
A1 Elena Rodriguez-Vieitez
A1 Stephen F. Carter
A1 Konstantinos Chiotis
A1 Laure Saint-Aubert
A1 Antoine Leuzy
A1 Michael Schöll
A1 Ove Almkvist
A1 Anders Wall
A1 Bengt Långström
A1 Agneta Nordberg
YR 2016
UL http://jnm.snmjournals.org/content/57/7/1071.abstract
AB The PET tracer 11C-deuterium-L-deprenyl (11C-DED) has been used to visualize activated astrocytes in vivo in patients with Alzheimer disease (AD). In this multitracer PET study, early-phase 11C-DED and 11C-Pittsburgh compound B (11C-PiB) (eDED and ePiB, respectively) were compared as surrogate markers of brain perfusion, and the extent to which 11C-DED binding is influenced by brain perfusion was investigated. Methods: 11C-DED, 11C-PiB, and 18F-FDG dynamic PET scans were obtained in age-matched groups comprising AD patients (n = 8), patients with mild cognitive impairment (n = 17), and healthy controls (n = 16). A modified reference Patlak model was used to quantify 11C-DED binding. A simplified reference tissue model was applied to both 11C-DED and 11C-PiB to measure brain perfusion relative to the cerebellar gray matter (R1) and binding potentials. 11C-PiB retention and 18F-FDG uptake were also quantified as target-to-pons SUV ratios in 12 regions of interest (ROIs). Results: The strongest within-subject correlations with the corresponding R1 values (R1,DED and R1,PiB, respectively) and with 18F-FDG uptake were obtained when the eDED and ePiB PET data were measured 1–4 min after injection. The optimum eDED/ePiB intervals also showed strong, significant ROI-based intersubject Pearson correlations with R1,DED/R1,PiB and with 18F-FDG uptake, whereas 11C-DED binding was largely independent of brain perfusion, as measured by eDED. Corresponding voxelwise correlations confirmed the ROI-based results. Temporoparietal eDED or ePiB brain perfusion measurements were highly discriminative between patient and control groups, with discriminative ability statistically comparable to that of temporoparietal 18F-FDG glucose metabolism. Hypometabolism extended over wider regions than hypoperfusion in patient groups compared with controls. Conclusion: The 1- to 4-min early-frame intervals of 11C-DED or 11C-PiB are suitable surrogate measures for brain perfusion. 11C-DED binding is independent of brain perfusion, and thus 11C-DED PET can provide information on both functional (brain perfusion) and pathologic (astrocytosis) aspects from a single PET scan. In comparison with glucose metabolism, early-phase 11C-DED and 11C-PiB perfusion appear to provide complementary rather than redundant information.