Background
Cross-sectional imaging studies suggest that patterns of hypometabolism (measured
by [18F] fluorodeoxyglucose positron emission tomography [FDG-PET]) and amyloid deposition
(measured by [11C] Pittsburgh Compound B [PiB]- PET) in Alzheimer's disease (AD) show some overlap
with each other. This indicates that neuronal dysfunction might spread within the
anatomical pattern of amyloid deposition. The aim of this study was to examine longitudinal
regional patterns of amyloid deposition and hypometabolism in the same population
of mild AD subjects and to establish their regional relationship to each other.
Methods
Twenty patients with mild AD underwent baseline (BL) and follow-up (FU) examination
with [18F] FDG-PET and [11C] PiB-PET. Voxel-by-voxel statistical group comparison (SPM5) was performed between
patient BL- and FU-PET data as well as between patients and 15 PiB-negative elderly
control subjects, who had undergone identical imaging procedures. To obtain objective
measures of regional overlap, Dice similarity coefficients (DSC) between the imaging
findings were calculated.
Results
Compared with elderly control subjects, AD patients showed typical patterns of BL
hypometabolism and BL amyloid deposition, with a similarity of 40% (DSC). Amyloid
deposition was more extended than hypometabolism at BL and showed only minor changes
over time, whereas significant expansion of hypometabolism was observed, almost exclusively
within areas already affected by BL amyloid deposition. Thus, increased similarity
of FU hypometabolism with BL amyloid deposition was found (DSC: 47%).
Conclusions
Longitudinal regional expansion of cerebral hypometabolism, as a measure of neuronal
dysfunction in AD, seems to follow the anatomical pattern of amyloid deposition with
temporal delay. This indicates that amyloid-based disruption of neuronal integrity
might contribute to the regional expansion of neuronal dysfunction.
Key Words
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Article info
Publication history
Published online: June 17, 2011
Accepted:
April 20,
2011
Received in revised form:
March 26,
2011
Received:
November 6,
2010
Identification
Copyright
© 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
