Pathogenic variants in the progranulin (GRN) and microtubule-associated protein tau (MAPT) gene and pathogenic G4C2 repeat expansions in chromosome 9 open reading frame 72 (C9orf72) are the most common causes.3 With promising avenues opening for clinical trials, research in the genetic FTD field has been increasingly moving toward the presymptomatic and early prodromal stages, in which the pathologic burden is still low.4 This highlights the importance of accurate cognitive screening in these early disease stages. This evidence concerns the gene MAPT and frontotemporal dementia.