We found that: (i) an important proportion of patients did not meet the molecular definition of AD and were thus classified as SNAP, with some of them having tau tracer binding limited to the entorhinal cortices and/or amygdala without amyloid deposition; (ii) SNAP patients were older and showed a lower ApoE ε4 allele frequency than AD patients but both groups had comparable isolated ASHT and a similar degree of medial temporal atrophy at baseline; (iii) disease progression differed in SNAP and AD patients regarding cognitive profile, brain atrophy and tau deposition patterns. This evidence concerns the gene MAPT and Brain atrophy.