Here, we further explored the synaptic plasticity disrupting actions of soluble synaptotoxic full-length tau aggregates prepared from recombinant protein, after either sonication of pre-formed fibrils (sonicated tau aggregates, SτAs) [11,22] or disulfide bond formation (oligomer-enriched tau, oTau) [9], and that present in aqueous extracts of neuropathological brain samples, including AD and the tauopathy of Pick’s disease (PiD) [23,24]. The gene discussed is MAPT; the disease is Alzheimer disease.