These deposits are mainly constitutedby neurofibrillary tangles of tau protein and amyloid plaques composedof 37–42 residue peptide, the amyloid β-peptide (Aβ),derived from the proteolysis of the Amyloid Precursor Protein (APP).8,9 According to the amyloid hypothesis, small oligomers or protofibrilsof Aβ peptides can be highly neurotoxic and ultimately produceneurodegeneration and loss of cognitive functions.10,11 In this framework, the retrieving of methods able to interfere withthe amyloid formation and reduce its effects in living systems canhelp in the design of new strategies against AD. The gene discussed is APP; the disease is Alzheimer disease.