Although PET has been proposed as a potential method of monitoring AD progression as well as responsivity to anti-inflammatory therapies (Jack et al., 2013), PET methods such as TSPO (translocator protein) imaging harbor a number of limitations including genotypic variation, complex tracer kinetics, and variability of plasma free fractions across human clinical cohorts (Turkheimer et al., 2015). This evidence concerns the gene TSPO and Alzheimer disease.