A study showed that PART patients had similar progression and seeding activity patterns across all neuropathological stages to AD patients despite having less Aβ deposition (Kaufman et al., 2018), which contrasts sharply with the higher seeding activity reported in plaque cases (Bennett et al., 2017), suggesting that the phosphorylated tau spread in early AD progression occurs in an Aβ-dependent or -independent manner. The gene discussed is MAPT; the disease is Alzheimer disease.