The lack of significant differences between presymptomatic and symptomatic MAPT mutation carriers likely reflects insufficient statistical power given the small sample size, or could reflect differences in underlying pathology (eg, tau pathology in MAPT-associated FTD vs TDP-43 pathology in GRN-associated and C9orf72-associated FTD).1 While these findings are novel in FTD, a few studies have identified reduced NPTXs in AD, both in brain and in CSF,12–19 although mostly through mass spectrometry approaches (box 1). The gene discussed is MAPT; the disease is Alzheimer disease.