Altogether, based on the accumulating data we suggest that there are perhaps two independent pathways of limbic/cortical tau spread that initiates with subthreshold levels of biomarker-measured pathology, converting to a minimal degree of pathology in either hippocampus/entorhinal cortex or association cortex (i.e., minimal tau subtype in PET studies, or minimal atrophy subtype in MRI studies [8]). The gene discussed is MAPT; the disease is Atrophy.