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. 2010 Sep;23(3):185-98.
doi: 10.1177/0891988710363715. Epub 2010 Apr 29.

Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18 F-FDG) PET in patients with Alzheimer disease, mild cognitive impairment, and healthy controls

D P Devanand  1 , Arthur Mikhno, Gregory H Pelton, Katrina Cuasay, Gnanavalli Pradhaban, J S Dileep Kumar, Neil Upton, Robert Lai, Roger N Gunn, V Libri, Xinhua Liu, Ronald van Heertum, J John Mann, Ramin V Parsey
Affiliations

Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18 F-FDG) PET in patients with Alzheimer disease, mild cognitive impairment, and healthy controls

D P Devanand et al. J Geriatr Psychiatry Neurol. 2010 Sep.

Abstract

Amyloid load in the brain using Pittsburgh compound B ((11)C-PIB) positron emission tomography (PET) and cerebral glucose metabolism using fluorodeoxyglucose ((18)F-FDG) PET were evaluated in patients with mild Alzheimer disease (AD, n = 18), mild cognitive impairment (MCI, n = 24), and controls (CTR, n = 18). ( 11)C-PIB binding potential (BP(ND)) was higher in prefrontal cortex, cingulate, parietal cortex, and precuneus in AD compared to CTR or MCI and in prefrontal cortex for MCI compared to CTR. For (18)F-FDG, regional cerebral metabolic rate for glucose (rCMRGlu) was decreased in precuneus and parietal cortex in AD compared to CTR and MCI, with no MCI-CTR differences. For the AD-CTR comparison, precuneus BP(ND) area under the receiver operating characteristic (ROC) curve (AUC) was 0.938 and parietal cortex rCMRGlu AUC was 0.915; for the combination, AUC was 0.989. ( 11)C-PIB PET BP(ND) clearly distinguished diagnostic groups and combined with (18)F-FDG PET rCMRGlu, this effect was stronger. These PET techniques provide complementary information in strongly distinguishing diagnostic groups in cross-sectional comparisons that need testing in longitudinal studies.

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Figures

Figure 1
Figure 1
11C-PIB PET BPND in Alzheimer’s Disease (AD), mild cognitive impairment (MCI), and healthy control subjects (CTR). BPND data were derived from regional analysis of MR coregistered 11C-PIB images using the Logan method with gray matter cerebellum as the reference region. CIN=cingulate, HIP=hippocampus, PFC=prefrontal cortex; PHG=parahippocampal gyrus, PAR=parietal cortex, PCN=precuneus. Non aMCI=non-amnestic MCI, aMCI=amnestic MCI.
Figure 2
Figure 2
18F-FDG PET rCMRGlu in Alzheimer’s Disease (AD), mild cognitive impairment (MCI), and healthy control subjects (CTR). rCMRGlu was derived from regional analysis of MR coregistered 18F-FDG PET images with ratio of each ROI to cerebellum represented on the y-axis. Non aMCI=non-amnestic MCI, aMCI=amnestic MCI. CIN=cingulate, HIP=hippocampus, PFC=prefrontal cortex; PHG=parahippocampal gyrus, PAR=parietal cortex, PCN=precuneus.
Figure 3
Figure 3
Comparison of CTR, MCI, and AD subjects’ BPND (left) and rCMRglu (right) data derived from PET 11C-PIB and 18F-FDG scans respectively. All PET data was non-linearly registered, using each individual’s MRI, to the SPM5 MNI single subject MRI template using the Automated Registration Toolbox (ART). MNI space BPND and rCMRGlu maps were averaged voxel-by-voxel in the AD (first row), MCI (second row), and CTR (third row) groups. The middle color bar represents the BPND (left side) and rCMRglu (right side) value in the images. Arrows point to regions of interest for the prefrontal cortex (PFC), precuneus (PCN), anterior cingulate (ACN), and hippocampus (HIP).
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