Lehmann M, Ghosh P, Madison C, Corbetta C, Long A, Miller B, Jagust W, Rabinovici G.
Diverging PIB and FDG Covariance Patterns Across Clinical Variants of AD.
Human Amyloid Imaging Abstract. 2012 Jan 1;
The current study aimed to assess patterns of covariance of PIB and FDG uptake in regions that are implicated in specific clinical presentations of AD.
The study included9 patients with probable AD (24 amnestic (AD-MEM) language (AD-LANG) and4 visual variants (AD-VIS), age =5.0 (9.4) years% male). In a previous study, peak atrophy voxels that showed selective grey matter atrophy in each AD variant compared with the other two were identified in: the right middle frontal gyrus in AD-MEM, the left superior temporal sulcus in AD-LANG, and the right middle occipital gyrus in AD-VIS.mm spheres were drawn around these voxels, and FDG and PIB values were extracted for each ROI. Multiple regressions were performed in SPM to assess correlations between FDG and PIB uptake in the ROIs with uptake at each voxel across the brain. Analyses were conducted with all subjects pooled together, adjusting for age, gender and education.
FDG uptake in the three ROIs produced distinct patterns of covariance (Figure A), with the regions involved for each ROI greatly overlapping with specific functional networks. Regions found to correlate with FDG in the AD-MEM region greatly overlapped with the default-mode network, whilst FDG uptake in the AD-LANG ROI mainly correlated with hypometabolism in left hemisphere regions typically associated with the language network, and FDG in the AD-VIS ROI correlated with regions of the ventral and dorsal visual processing networks. In contrast, PIB uptake in the three ROIs showed diffuse covariance patterns across the brain, with great overlap between the three correlation maps (Figure B).
Regions targeted in AD clinical variants showed distinct FDG covariance patterns that corresponded with expected functional networks, whereas PIB uptake covaried diffusely across the brain. We hypothesize that AD syndromes are associated with degeneration of specific networks, and that anatomic differences between AD variants are not explained by distinctions in the regional deposition of amyloid.