P-glycoprotein function is associated with a number of neurodegenerative and
psychiatric diseases as well as with pharmacoresistance to for example antiepileptic drugs.
The ability to measure P-gp function in vivo would allow for an increased understanding of
the mechanisms of disease and treatment. This review assesses the various approaches to in
vivo quantification of P-gp function using currently available P-gp tracers and PET in humans.
First, the use of compartment models, and their interpretation in terms of P-gp function
at the blood-brain barrier, is discussed. Then, the methods that have been used to quantify
PET data of the P-gp tracers [11C]verapamil, [11C]N-desmetyl-loperamide (dLop),
[11C]laniquidar, [11C]phenytoin, [11C]tariquidar and [11C]elacridar are reviewed. In summary,
the extraction of P-gp substrate PET tracers, which is their plasma to tissue rate constant K1
corrected for variations in regional cerebral blood flow, is generally considered to be the
preferred measure of P-gp function.