Several studies of the amyloid-β protein aggregates, which cause AD, also indicate that the existence of distinct shapes in beta amyloid peptide (Aβ) aggregates, 40 residue Aβ (Aβ40) and 42 residue Aβ fibril structures [51], and identify the distinct strain-specific traits (defined as “strainness”) of the forms of AD by the different conformation of the aggregates [91, 104]. This evidence concerns the gene APP and Alzheimer disease.