MAPT and Alzheimer disease: Indeed, evidence for structural variation in amyloid-β fibrils from distinct clinical subtypes of AD has been reported12, and remarkable recent progress with structural characterization of diverse self‐propagating assemblies of tau, amyloid‐β, α‐synuclein and TDP-43 from human brain is now facilitating the detailed exploration of the role for strains in determining phenotype16–19.