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Fig. 8 | Molecular Neurodegeneration

Fig. 8

From: The release and trans-synaptic transmission of Tau via exosomes

Fig. 8

Exosomes isolated from CSF of AD or control subjects contain Tau and induce TauRDΔK aggregation. a The presence of Tau monomers and trimers in exosomes determined with western blots. Besides Tau monomers, Tau trimers (indicated by arrowheads, top right) ran around 180kD were detected in both exosomes from AD and controls. These Tau trimers were phosphorylated at 12E8 sites (a2) and PHF1 (a3). Two Tau monomer bands were also phosphorylated at PHF1 sites and 12E8 sites (indicated with arrows). Between the phosphorylated Tau monomer bands, other Tau bands were not phosphorylated at PHF1 and 12E8 sites (a1, indicated by *). b Tau in CSF before isolation of exosomes. Monomeric Tau (doublet between Mr 55-70kD (indicated by arrows), but no Tau oligomers of ~180kD was detected. c Quantification of Tau shown in a. No significant differences of the amount of total Tau (c1) and Tau phosphorylated at 12E8 sites (c2) and PHF1 sites (c3) were observed between exosomes isolated from AD and controls. Error bars: SD. Student t-test: n.s., not significant. d Diagram showing the luciferase protein-fragment complementation assay. N2a cells were co-transfected with TauRDΔK fused to split luciferase constructs (N: N-terminal part of luciferase, C: C-terminal part of luciferase). A luminescence signal is only detected after complementation of both split luciferase fragments (e.g. during dimerization and oligomerization of TauRDΔK) and indicates the induction of TauRDΔK aggregation. e Promotion of TauRDΔK aggregation by exosomes from human CSF. Luminescence increases in reporter cells upon treatment with exosomes prepared from equal volumes of CSF from AD (n = 13) or controls (n = 13). All measurements were performed in triplicates. **, p < 0.001, n.s., non-significant, one way ANOVA

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