Evaluation of the associations between [11C]PIB and [18F]AV1451 PET retention and MRI atrophy in Alzheimer’s Disease

2016 
18 Objectives To study, at both the voxel- and ROI levels, the associations between amyloid and tau accumulation (measured by PET) and their effects on neurodegeneration (measured with MRI) in patients with Alzheimer’s Disease (AD). Methods We included twenty-seven patients (mean age 63±8.6 yrs, MMSE 22±4.9) with a clinical diagnosis of probable AD and positive amyloid (11C-PiB) PET. All patients underwent a 3T T1-weighted MRI, 11C-PiB-PET and 18F-AV1451-PET. 11C-PiB 90-minutes DVR images and 18F-AV1451 80-100 minutes SUVR images were created using cerebellar gray matter reference region and warped to a standard space along with the respective segmented gray matter masks. Seven meta-ROIs (frontal, cingulate, parietal, lateral/medial temporal, lateral/medial occipital) were created from Freesurfer-defined ROIs and used to extract gray matter probabilities (GMP), 11C-PiB DVR and 18F-AV1451 SUVR. Partial Volume correction at the voxelwise level was applied following a 3-compartment method. Associations between PET biomarkers were estimated with PVC-data at the voxel-level with Biological Parametric Mapping (BPM) voxel-wise robust regression modeling, covarying for age and gender. Subsequently, further BPM analyses were run to estimate correlations between each PET biomarker and neurodegeneration, adding total intracranial volume (TIV) as a further nuisance covariate. The same associations were evaluated at the ROI-based level. Results Voxelwise BPM analysis showed significant correlations (p Conclusions These findings show significant associations between tau and amyloid accumulation in signature AD pathology regions. Brain atrophy appeared to be significantly associated only with tau accumulation. The difference between intra-modality correlations (higher relationships for 11C-PiB than 18F-AV1451) is likely to reflect greater regional-specificity of tau vs. diffuse and inter-correlated accumulation of cortical amyloid at the dementia stage.
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