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01.06.2014 | Original Article | Ausgabe 6/2014

European Journal of Nuclear Medicine and Molecular Imaging 6/2014

The effect of amyloid pathology and glucose metabolism on cortical volume loss over time in Alzheimer’s disease

Zeitschrift:
European Journal of Nuclear Medicine and Molecular Imaging > Ausgabe 6/2014
Autoren:
Sofie M. Adriaanse, Koene R. A. van Dijk, Rik Ossenkoppele, Martin Reuter, Nelleke Tolboom, Marissa D. Zwan, Maqsood Yaqub, Ronald Boellaard, Albert D. Windhorst, Wiesje M. van der Flier, Philip Scheltens, Adriaan A. Lammertsma, Frederik Barkhof, Bart N. M. van Berckel

Abstract

Purpose

The present multimodal neuroimaging study examined whether amyloid pathology and glucose metabolism are related to cortical volume loss over time in Alzheimer’s disease (AD) patients and healthy elderly controls.

Methods

Structural MRI scans of eleven AD patients and ten controls were available at baseline and follow-up (mean interval 2.5 years). Change in brain structure over time was defined as percent change of cortical volume within seven a-priori defined regions that typically show the strongest structural loss in AD. In addition, two PET scans were performed at baseline: [11C]PIB to assess amyloid-β plaque load and [18F]FDG to assess glucose metabolism. [11C]PIB binding and [18F]FDG uptake were measured in the precuneus, a region in which both amyloid deposition and glucose hypometabolism occur early in the course of AD.

Results

While amyloid-β plaque load at baseline was not related to cortical volume loss over time in either group, glucose metabolism within the group of AD patients was significantly related to volume loss over time (rho = 0.56, p < 0.05).

Conclusion

The present study shows that in a group of AD patients amyloid-β plaque load as measured by [11C]PIB behaves as a trait marker (i.e., all AD patients showed elevated levels of amyloid, not related to subsequent disease course), whilst hypometabolism as measured by [18F]FDG changed over time indicating that it could serve as a state marker that is predictive of neurodegeneration.

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