A recent PET-based study showed that the magnitude and topography of tau deposition were closely related to the duration of amyloid deposition in preclinical and symptomatic individuals and supported the notion that the combination of Aβ and tau is required for accelerated longitudinal cognitive decline in preclinical AD.22 The same study showed, however, that individuals with mild cognitive impairment can have Aβ positivity with low or no PET stage of tau deposition; furthermore, this discrepancy was seen in a few cases with dementia.22 This evidence concerns the gene MAPT and dementia.