We aimed in this study to characterize the cerebral uptake pattern of [18F]-APN-1607 as a marker for hyperphosphorylated tau in patients with clinically diagnosed AD in comparison to a normal control (NC) group and to investigate the correlation of this regional uptake with hypometabolism to [18F]-FDG PET and in relation to impaired cognitive function. This evidence concerns the gene MAPT and Alzheimer disease.