Specifically, we examined the degradation of amyloids accumulating in the bodies of patients with Alzheimer’s disease (formed from abeta peptide (1-42)) [55, 56], Parkinson’s disease (formed from alpha-synuclein) [57–59], hemodialysis amyloidosis in acute renal failure (formed from beta-2-microglobulin) [60, 61], and systemic lysozyme amyloidosis (formed from lysozyme) [62, 63]. This evidence concerns the gene B2M and Alzheimer disease.