In both neurodegenerative conditions, amyloidogenic proteins (typically, Aβ and the microtubule-associated protein tau in AD, and αS in PD) misfold and self-assemble via a nucleated-growth mechanism to form transient, low-molecular-weight soluble oligomers, later converting into β-sheet-rich protofibrils and finally stabilize as highly ordered fibrillar structures. This evidence concerns the gene MAPT and Alzheimer disease.