"<a href=""https://www.youtube.com/watch?v=Gfr50f6ZBvo&amp;t=44m12s"">44:12</a> pretty sure he meant Tau protein", as it’s the one hypothesized to have this pathological, gain of function structure that templates the folding of naïve Tau proteins in a prion-like manner. These then go on to form neuronal fibrillary tangles that disrupt cell function. The interesting thing is that, even according to AlphaFold, mammalian Tau is INTRINSICALLY disordered. So the big question is: how the hell does it become so suddenly metastable? Template OTHER proteins? Certainly ABeta is involved, but the landscape of all possible “stable” conformations in the context of Alzheimer’s is such an interesting field of study — one that will hopefully lead us to a cure someday.