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. 2020 Nov 27;144(1):288–309. doi: 10.1093/brain/awaa376

Figure 2.

Figure 2

PK treatment of human brain derived EVs for biochemical characterization. (A) Workflow of the tau purification by sequential centrifugation after with or without PK treatment. (B) Western blot analysis of non-treated and PK-treated EVs from three groups (CTRL, pAD and Alzheimer’s disease) with CD63 and actin antibodies. (C) Immunoelectron microscopy images of ultrathin-sectioned Alzheimer’s disease EVs for PHF1+ tau with or without PK-treatment. Images were captured at direct magnification ×30 000, with the 10 nm immunogold labelling. (D) Western blot analysis of oligomer-enriched (S1p) and sarkosyl-insoluble tau-enriched (P2) fractions from EVs for PHF1 with or without PK-treatment. (E) Semi-quantification of PHF1 immunoreactivity. Two donors per group for CTRL and pAD and four donors for the Alzheimer’s disease group. (F) Immunoelectron microscopy of isolated tau fibrils, oligomers or sarkosyl-insoluble fraction of EVs from human Alzheimer’s disease brain tissue. Images were captured by TEM at direct magnification ×40 000, with the 5-nm immunogold labelling for PHF1. (A–F) Donors 1 and 2 (control, CTRL), 4 and 5 (pAD), and 7–10 (Alzheimer’s disease, AD) were used (Supplementary Table 2).