Fig. 7

Schematic representation of data discussed in the presented research highlighting two main outcomes. In wild-type primary mouse neurons, aggregation of endogenous mouse tau is triggered by human AD-tau and more importantly, the aggregation properties of mouse tau (rate and conformation) are linked to the conformational diversity of the original individual AD cases used as inoculum. Thus, the propagation of misfolding and aggregation from human AD-tau to mouse tau occurs in a prion-like manner, and the diversity of human AD-tau species across individual AD cases can be transferred to primary neurons to model AD pathogenesis and its consequences at the level of cellular structures and mechanisms. The propagation of tau aggregation affects the synapses. The neurons with triggered tau pathology show reduced levels of synaptic connections, which may be linked to the disruption of the post-synaptic compartment and decreased levels of post-synaptic scaffolding proteins