The most investigated molecular event associatedwith cell death is the aggregation of amyloid-β (Aβ, hereafter)peptides to form extracellular fibrils.1−6 Aβ peptides are the byproduct of amyloid precursor protein(APP).7 The relative abundance of amyloidpeptides in both normal subjects and AD patients is still debated.8,9 Recent analyses reported the ranking of abundance as Aβ(4-42)∼ Aβ(1-42) > Aβ(1-40), with strong indicationsof Aβ(4-42) peptide as the most abundant in AD patients (seeref (10) and discussiontherein). This evidence concerns the gene APP and Alzheimer disease.