. Regional expansion of cerebral hypometabolism in AD follows the pattern of amyloid-deposition with temporal delay and is related to a healthy functional connectivity network. Human Amyloid Imaging 2011 Meeting Abstracts. 2011 Jan 15;

Abstract:

Background: Hypometabolism and amyloid-deposition in AD show some regional overlap with each other and with the healthy gdefault-modeh network (DMN) of functional connectivity. This indicates that neurodegeneration may spread within anatomical borders defined by functional connectivity networks (FCN). Aim was to examine longitudinal regional patterns of amyloid-deposition and hypometabolism in the same population of AD patients and to establish their regional relationship to each other and to healthy FCNs.

Methods: Twenty patients with mild AD (67.7} 7.9 yrs) underwent baseline (BL) and 2-year follow-up (FU) [18F] FDG- and [11C]PIB-PET. SPM5 voxelwise group comparisons were performed between patientsf BL- and FU-data and between patients and 15 elderly controls (64} 5 yrs), which had undergone identical imaging procedures. Areas of maximum BL-amyloid-deposits in patients were used as seed regions for calculation of a FCN in a resting-state fMRI dataset from 27 young controls (24} 4 yrs). Dice similarity coefficients (DSC) between imaging findings were calculated (significance threshold p Results: Compared to elderly controls, AD-patients showed typical patterns of BL-hypometabolism- and amyloiddeposition, with a DSC of 40%. At BL amyloid-deposition was more extended than hypometabolism and showed only minor regional expansion, whereas prominent expansion of hypometabolism was observed, primarily within areas already affected by BL-amyloid-deposition; thus, increased DSC (47%) of FU-hypometabolism with BLamyloid- deposition was found. The FCN calculated in young controls (using BL-amyloid-peaks in AD as seed regions) showed higher similarity with FU-hypometabolism in patients than standard DMN (DSC 45% vs. 26%).

Conclusions: Regional expansion of hypometabolism, as a measure of neuronal dysfunction in AD, appears to follow the anatomical pattern of amyloid deposition with temporal delay. Accurate prediction of FU-hypometabolism was possible by using BL-amyloid-peaks found in AD to seed a healthy FCN, such that amyloid-based disruption of functional networks may contribute to the regional expansion of neuronal dysfunction.

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