We chose young (7 months) rats, an age which is early in relation to the evolution of the AD pathology in this model, but at which there are already increased levels of Aβ-42 oligomers, Triton soluble Aβ-40 and total Tau (sarkosyl-soluble and crude pellet).21,25 Using [18F]FDG-PET, we found a modest but significant decrease in glucose uptake in the frontal association cortex of Tg rats vs WT, a region only associated with hypometabolism in the later stages of clinical AD,32 but no differences in other regions. The gene discussed is MAPT; the disease is Alzheimer disease.