Notably, some mutation carriers already passed their estimated age of onset by more than 5 years, suggesting that these subjects have a high resilience against Alzheimer’s disease-related pathology, for instance due to a large cognitive reserve attributed to a relatively high level of education124 or protective genes.125 Additionally, the lack of amyloid and tau biomarker status determination close to MEG registration prevented direct correlation of functional brain network abnormalities to protein aggregates. Here, MAPT is linked to Alzheimer disease.