In the AD affected brain a second pathway, known as the “amyloidogenic pathway”, is activated, involving the sequential action of β-secretase (or beta-site amyloid precursor protein cleavage enzyme [BACE1]) and γ-secretase, to generate two predominant Aβ peptides, either 40 or 42 amino acids in length, that are able to aggregate into fibrils via soluble oligomers, leading, as generally accepted, to neuronal toxicity. This evidence concerns the gene BACE1 and Alzheimer disease.