Fig. 5

Fixed human brain samples with tau pathology exhibit seeding activity. AT8-immunostained (hyperphosphorylated tau, DAB) 100 μm sections from cases 3 (a) and 4 (b) in Table 3. In NFT stage III, the tau pathology in the hippocampal formation increases. a,b. The entorhinal layers pre-α and, in addition, pri-α become heavily involved. Tau pathology extends through the transentorhinal region into the adjoining high order sensory association areas of the temporal neocortex but not yet into the superior temporal gyrus. c The NFT in the late stage V case shown here is not identical to case 5 in Table 1 but is from another Alzheimer’s disease patient in her eighties. During NFT stage V, tau lesions develop in the superior temporal gyrus and progress into first order sensory association and premotor areas of the neocortex. d Fixed tissue was isolated from the transentorhinal cortex and the hippocampus (CA1/3) of 100 μm human brain sections that were blinded prior to collection (Table 3). Samples were homogenized and transduced into tau biosensor cells. The integrated FRET density was normalized to a negative control treated only with Lipofectamine. Error bars = S.E.M, ** = p < 0.01, **** = p < 0.0001