The amyloid hypothesis has been the dominant theory for the cause of Alzheimer’s disease for over 20 years. In brief, the theory holds that Alzheimer’s disease is caused by the accumulation of beta-amyloid that damages nerve cells in the brain. Beta-amyloid is cleaved from the large amyloid precursor protein (APP) into two main peptides that are released outside the cell, beta-amyloid 40 and beta-amyloid 42, containing respectively 40 and 42 amino acids. According to the amyloid hypothesis, in normal people, these peptides are rapidly removed, but in people with Alzheimer’s disease the metabolic ability to degrade them is decreased, the peptides accumulate, form fibrils, and ultimately solid amyloid plaques that in turn damage neurons and trigger the formation of abnormal tau pathology causing neuronal death.