Although there are inter-individual differences in typical AD, the spatial heterogeneity of tau is generally limited,7,8,19,29 and largely adheres to the Braak staging scheme of tau pathology with a strong emphasis on medial and lateral aspects of the temporal lobe.1,30-34 Therefore, a crucial test of the connectivity-progression hypothesis is to determine whether connectivity-based tau progression models can be generalized to clinical phenotypes with other tau deposition patterns extending beyond the temporal lobe. This evidence concerns the gene MAPT and Alzheimer disease.