Recent studies have shown that Aβ plaques and tau protein aggregates in the brains of AD patients have distinct individual and subtype-specific structural differences, a phenomenon known as “strain.” This conformational diversity alters the pathogenicity and spread of aggregates in the brain, and this structural change can make biomarker detection extremely difficult, as conventional diagnostic tests may not detect all forms of aggregates (107). This evidence concerns the gene MAPT and Alzheimer disease.