Amyloid-β (Aβ) proteins of residues 40 and 42 and tau isoforms of residues 352–421, which are linked to Alzheimer’s disease (AD), have the propensity to aggregate into amyloid fibrils with a cross-β structure [1,2] and multiple polymorphs, as observed by Scheres et al. and Tycko et al. [3,4]. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.