Section 2.3.2 and Section 2.4.2 above describe in vitro and in vivo AD studies demonstrating the molecular relationship between iron and tau deposition in the context of Hypotheses 1 and 2, whose findings may be relevant to PSP as well. Specifically, in the context of PSP—a 4R tauopathy—a study using recombinant 4R2N tau revealed ferric-iron-specific inducement of tau oligomerization and fibrils in a dose-dependent manner, both with and without heparin. Moreover, the binding affinity of ferric iron was observed to be four times greater than that of ferrous iron [96]. The gene discussed is MAPT; the disease is Alzheimer disease.