Following biochemical fractionation and subsequent immunoblotting of the soluble S1 fraction, consistent with the TauA152T-AAV model we observed robust accumulation of soluble pT153-positive tau species in A152T carriers relative to noncarriers in AD (Fig. 5c), PSP (Additional file 1: Figure S5a), as well as LBD, CBD and FTLD-MND (Additional file 1: Figure S5b). This evidence concerns the gene PSMD1 and Alzheimer disease.