A possible explanation for the higher risk of developing Alzheimer’s disease in T2DM is that: (1) Neprilysin, an enzyme degrading amyloid-β, has another target protein for degradation, insulin; (2) T2DM patients exhibit hyperinsulinemia; (3) in T2DM patients with hyperinsulinemia, neplilysin contributes to degradation of insulin in addition to amyloid-β, resulting in less amyloid-β degradation by neplilysin than in healthy individuals; (4) this process increases the accumulation of amyloid-β [106,107,108]. This evidence concerns the gene INS and Alzheimer disease.