Amyloid peptides (Aβs), found in extraneuronal plaques in AD patients as well as in intraneuronal compartments, result from the amyloidogenic proteolytic cleavage of Amyloid Precursor Protein (APP) by the sequential action of β- and γ-secretase enzymes, and a significant body of evidence suggests that Aβ accumulations in AD are the result of an imbalance between Aβ production and Aβ clearance [97–99]. This evidence concerns the gene DDX41 and Alzheimer disease.