Remarkably, it has been shown that the tau protein can self-assemble into a range of different amyloid structures, known as polymorphs, in a pathology-dependent manner, including in AD, Pick’s disease (PiD), chronic traumatic encephalopathy (CTE), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP) [4, 135] (Table 1), and the same is true for amyloid fibrils formed from other proteins [137]. The gene discussed is MAPT; the disease is Alzheimer disease.