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FDG and Amyloid Positron Emission Tomography

Published online by Cambridge University Press:  07 November 2014

Mark A. Mintun
Mark A. Mintun*
Affiliation:
Dr. Mintun is professor of radiology with joint appointments in psychiatry, neurobiology and biomedical engineering; interim director of radiological science; director of the Center for Clinical Imaging Research; and director of the Division of Research Development, at, Washington University, School of Medicine in St. Louis, Missouri
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Extract

For over 20 years, researchers have used the tracer [18F]fluorodeoxyglucose (FDG) in positron emission tomography (PET) imaging. FDG PET imaging has been utilized to study the characteristic metabolic changes in Alzheimer’s disease (AD), and as more molecular imaging tracers become available for human research, PET will likely assume many new roles for investigating more specific abnormalities, such as amyloid deposition, in the future.

FDG is a glucose analog that images glucose metabolism and also illustrates neural firing. Different synapse activity, particularly excitatory activity from glutamate release, appears to change FDG uptake. AD will affect both brain infrastructure by decreasing the amount of cell bodies and synapses as well as decreasing synaptic activity, which are both changes that decrease the amount of FDG. AD is not a perfectly uniform process, and this is reflected by distinct progressive patterns of decreased FDG and decreased metabolism across different regions of the brain.

FDG enters the brain via blood flow, and then into brain tissue by both diffusion and facilitated transport. Once it enters the glia and neurons, FDG can be phosphorylated, a step that is essentially irreversible, but then cannot be processed further by the cells, effectively trapping the FDG in situ. The amount of trapping that occurs in the brain over the first 10–20 minutes is very high and constitutes over 80% of the uptake. Thus, after the first 10–20 minutes uptake phase, a pattern of FDG emerges that mirrors the distribution of glucose metabolism in all subcortical and cortical structures.

Type
Research Article
Information
CNS Spectrums , Volume 13 , Issue S16 , 2008 , pp. 21 - 24
Copyright
Copyright © Cambridge University Press 2008

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