Purpose
We aimed to develop a computational simulation model for β-amyloid (Aβ) positron emission tomography (PET) imaging.
Procedures
Model parameters were set to reproduce levels of Aβ within the PDAPP mouse. Pharmacokinetic curves of virtual tracers were computed and a PET detector simulator was configured for a commercially available preclinical PET-imaging system.
Results
We modeled the effects of Aβ therapy and tracer affinity on the ability to differentiate Aβ levels by PET. Varying affinity had a significant effect on the ability to quantitate Aβ. Further, PET tracers for Aβ monomers were more sensitive to the therapeutic reduction in Aβ levels than total brain amyloid. Following therapy, the decrease in total brain Aβ corresponded to the slow rate of change in total amyloid load as expected.
Conclusions
We have developed a first proof-of-concept Aβ-PET simulation model that will be a useful tool in the interpretation of preclinical Aβ imaging data and tracer development.