generated from a parent protein called the amyloid precursor protein (APP), which is cleaved in two steps by the enzymes β then γ secretase, leading to release of the Aβ fragment [119]. This is a normal physiological process that is modified in the disease state. Interestingly, inflammation can promote accumulation of Aβ by elevating APP levels and the activity of cleavage enzymes [120]. These observations have led to the inflammatory cascade hypothesis of Alzheimer’s disease, which states that Aβ deposition induces neuroinflammation, which in turn generates more Aβ, resulting in a vicious cycle [120].
